Gori buying ganja

__________________________

📍 Verified store!

📍 Guarantees! Quality! Reviews!

__________________________

▼▼ ▼▼ ▼▼ ▼▼ ▼▼ ▼▼ ▼▼

▲▲ ▲▲ ▲▲ ▲▲ ▲▲ ▲▲ ▲▲

Gori buying ganja

Official websites use. Share sensitive information only on official, secure websites. This is an open access article distributed under the Creative Commons Attribution License 4. The current rate of opioid prescription is disquieting because of their high abuse potential, adverse effects, and thousands of overdose deaths. This situation imposes urgency in seeking alternatives for adequate pain management. From this perspective, this study aimed to evaluate the experience and the perceived analgesic efficacy of medical cannabis in managing the pain associated with musculoskeletal conditions. A question survey was distributed to patients at a major medical cannabis center in Puerto Rico for 2 months. Demographics, medical history, cannabis usage, cannabis use perspective, and analgesic efficacy were assessed in the questionnaire. One hundred eighty-four patients completed our survey. This study showed an average pain reduction score of 4. Those with musculoskeletal conditions reported a notable average pain reduction score of 4. This study demonstrated that the use of medical cannabis among patients with musculoskeletal conditions effectively reduced pain levels based on their Numeric Rating Scale reported scores. The increasing use of opioids for pain management has raised concerns about their potential abuse and dangerous adverse effects. Orthopaedic surgeons represent close to 10 percent of opioid prescriptions. Especially considering that adequate postoperative pain management is a major determinant of patient satisfaction. Unfortunately, these medications have a notable risk for addiction and have been associated with adverse effects such as nausea, vomiting, constipation, and respiratory depression. In , Nazzal 6 reported no increase in pain scores or opioid consumption with prescription of lower doses of oxycodone after anterior cruciate ligament reconstruction, suggesting that achieving adequate pain control with lower doses is feasible. Finding non-narcotic alternatives with a better safety profile has been a research challenge. Previous studies have contemplated viable options to substitute opioids for pain management. Their protocol consisted of using gabapentin, acetaminophen, and an ultrasonography-guided interscalene block with 0. The study concluded that the complete elimination of opioid use by two weeks could be achieved with nonopioid-based alternative pain management because patient satisfaction did not diminish. In another study, a mg intravenous IV tramadol dose was shown to be safe and well tolerated for postoperative pain management, where traditional IV opioids are often used. Among the potential opioids surrogates, cannabis has been a poorly studied alternative because of its social stigma and limited access. Nonetheless, cannabis has gained considerable attention as a treatment alternative for different diseases such as multiple sclerosis, cancer-related emesis, anorexia, and cachexia. These constituents are found in plants belonging to the Cannabis genus, such as Cannabis indica , Cannabis sativa , and Cannabis ruderalis. Cannabinoids are classified as phytocannabinoids derived from plants, endocannabinoids are produced endogenously in the body, and synthetic cannabinoids are created artificially. The endocannabinoid system has shown promising results as an analgesic and anti-inflammatory pathway. CB1 receptors are associated with nociceptive areas of the central and peripheral nervous systems while CB2 receptors have shown the capability to suppress pain and inflammation. Medical cannabis can be administered through different methods; the most common routes are inhalation and oral ingestion. Moreover, cannabis could be administered through lotions, cartridges, concentrates, and sublingual drops. In , Romero-Sandoval et al 20 evaluated the analgesic effects of medical cannabis in patients with chronic pain. However, additional studies are necessary to understand the use and efficacy of medical cannabis as an adequate therapeutic alternative in pain management. Many strategies have been studied to reduce postoperative pain and avoid the opioid crisis, yet cannabis remains poorly assessed. This study aims to elucidate whether medical cannabis represents a satisfactory alternative for pain management in musculoskeletal disorders in a Hispanic population. A cross-sectional study was designed to assess the perceived efficacy of cannabis as an analgesic alternative in musculoskeletal conditions. The study population consisted of patients of a major medical cannabis center in Puerto Rico with multiple locations throughout the island. The dispensaries operate under the 42 to Law of the Government of Puerto Rico to market cannabis and its derivates for medical purposes, the sole approved use in the territory. All patients of the dispensaries meet the inclusion criteria consisting of age 21 years and older and having a valid license for medical cannabis use. However, patients of other medical cannabis centers were excluded to ensure that their products do not have a different formulation than the selected dispensaries. Enrollment in this study was voluntary and subject to written informed consent before participating. We prepared a question survey that was reviewed and approved by the senior author Figure 1. The anonymous questionnaire was administered at the dispensaries for a participation period of two months. The research personnel approached potential participants at the dispensaries' security checkpoint verify for valid cannabis license and extended an invitation to participate after fully disclosing the study objectives, including risks and benefits. Survey sheets were provided to all the patients who gave consent with instructions to fill the document and return it at the end of their appointment. The data assessed in the questionnaire included demographics, medical history medical conditions, allergies, and medications , toxic habits tobacco, alcohol, or non-cannabis drugs , cannabis usage questions, cannabis perspective questions, and an analgesic efficacy evaluation using the Numeric Rating Scale NRS. The NRS score before cannabis use and the NRS score reported after cannabis use were compared to assess the analgesic efficacy of cannabis as a potential alternative for pain management. In addition, information regarding their last four digits of phone number and initials were requested to avoid multiple participation because some patients frequently visit these dispensaries. Categorical data were evaluated using Pearson chi square and continuous data with analysis of variance. The Fisher exact test evaluated categorical data sets in groups with low-frequency counts. Descriptive analysis was done by analyzing frequencies, mean, and SD. This study was approved by the Institutional Review Board at our academic center. Two hundred and thirteen patients meeting our inclusion criteria were invited to participate in this study. The average age of the participants was Their average body mass index was The demographic data is summarized in Table 1. The reported medical indications for cannabis use were extensive. The reported conditions include anxiety disorders , insomnia , and musculoskeletal disorders 77 Table 3. These values are consistent with the fact that more than one condition could be included when licensing for medical cannabis. Among the participants, They were considered a subgroup for additional analysis Figure 1. Pie chart demonstrating the distribution of medical cannabis product formulations used by the respondents. NRS was used to assess and compare pain levels before and after using medical cannabis. The average pain reduction of the study participants was 4. The evaluation of the musculoskeletal disorder subset showed a significantly higher average pain reduction score 4. Contrarily, when the musculoskeletal disorder subset was removed from the data set, the average pain reduction score was lower but remained statistically significant 3. Our results demonstrate that medical cannabis patients perceived this drug ie, cannabis as an effective pain management alternative for musculoskeletal pain based on their NRS reported scores. In addition, most participants perceived medical cannabis as a better alternative than narcotics to attain adequate pain control. Currently, the dependence and abuse of opioids are a growing dilemma. It has been estimated that million opioids are prescribed annually in the United States, an increasing problem over the past 20 years. Therefore, exploring effective and safer alternatives is crucial to fighting the opioid pandemic. Medical cannabis is a promising alternative for replacing opioids. Owing to its theoretical anti-inflammatory and analgesic properties, this group of compounds ie, cannabinoids represents a potential pain management strategy. Cannabis is a drug that has become increasingly popular in recent years. Despite their Schedule 1 drug category, it is important to note that certain states have legalized both recreational and medicinal use of cannabis. Knowing the most common reasons for cannabis use can provide valuable information about the most common tendencies for using this drug and further determine its effectiveness. In a study done by Cahill et al, 22 the most common diseases for which the participants reported cannabis use were anxiety In a cross-sectional study by Lucas et al, 19 chronic pain Those results have certain similarities to our findings, where the most common reasons for medical cannabis use were anxiety, insomnia, chronic pain, and muscle spasms. In the perioperative setting, the surgeons and anesthesiologists must consider all aspects of cannabinoids usage. Anecdotal reports have detailed high anesthetic requirements, and a recent study reported an increase in propofol doses required to achieve successful laryngeal mask insertion and intubation. Some studies describe the effects of cannabis use in patients undergoing hip and knee arthroplasty. They report increased complication rates characteristic of IV drug administration as opposed to inhalation or ingestion. However, this study was not limited to cannabis use alone. Law et al 32 showed a lower rate of periprosthetic fracture, mechanical loosening, implant failure, and osteolysis as a cause of total knee arthroplasty revisions in the cannabis-user group. These findings did not reach statistical significance, which can be partially explained by studies investigating the effect of upregulating cannabinoid receptors CBs of the skeleton in mice. Activating the CB2 receptor stimulated bone formation, balanced bone remodeling, and perhaps played a protective role against age-related bone loss. A recent review analyzed data from the Healthcare Cost and Utilization Project Nationwide Inpatient Sample database to evaluate the effect of marijuana use by orthopaedic patients on inpatient mortality, heart failure, stroke, and cardiac disease. A decreased mortality rate was seen in patients who used marijuana. Clinical trials have investigated some of the most common indications for the therapeutic use of cannabinoids, including posttraumatic stress disorder, anxiety, sleep, and schizophrenia. Currently, there is insufficient evidence to estimate efficacy in these areas. Among the cannabis indications examined, acute and chronic pain management remains the most pertinent for orthopaedic surgery patients. This application represents a vital asset in the fight against the opioid crisis. Opioid use for pain management is a critical component in postoperative settings. However, there is an urgent need to seek less dangerous and addictive drugs. Corroborating the efficacy of medical cannabis compared with opioids is necessary to establish a proper relationship between cannabis and its analgesic effects. A study conducted by Perron et al 37 showed that efficacy ratings for pain management among cannabis users were higher compared with prescription pain medication users. By contrast, a pilot study conducted by Romero-Sandoval et al 20 demonstrated that oral THC had no effect on opioid consumption and had no positive effect on pain levels. After surgery, participants reported that consuming a synthetic cannabinoid drug nabilone produced higher pain scores than placebo. According to Lucas et al, 19 participants in their study who substituted cannabis for opioids reported a The main reasons for using cannabis over opioids were that patients considered cannabis to be a safer alternative to prescription drugs Similar to the studies by Perron et al 37 and Lucas et al, 19 our study demonstrated an overall pain reduction of 4. In , Brady et al evaluated the self-efficacy of medical cannabis patients in the context of researching, procuring, and using cannabis. Their study defines self-efficacy as an individual's belief in their capacity to produce a certain outcome. In this context, he observed that those patients with higher self-efficacy about medical cannabis were more likely to engage in activities to experiment and incorporate medical cannabis into their medical management despite the perspective of their providers about this treatment modality. This study has some limitations. First, using a questionnaire as a research tool imposes intrinsic restrictions such as differences in questions interpretation, dishonesty, unconscientious responses, or uncertain answers. Second, because more than one condition could be reported for medical cannabis licensing in our territory, there were some constraints in evaluating a group limited solely to musculoskeletal disorders. Third, the reported VAS score could have been affected by recall bias. Finally, medical cannabis is produced in varying quality, consumed in different quantities, and available through different brands providing some heterogenicity between patients that could influence the perceived efficacy among the participants. Future studies should assess these heterogenic features ie, dosages, quality, and brands to guide medical professionals toward a more accurate prescription for medical cannabis. Medical cannabis is an understudied drug with theoretical analgesic properties that could represent an asset against the current opioid pandemic. This study showed that the use of medical cannabis among patients with musculoskeletal conditions effectively reduced pain levels based on their NRS reported scores. In addition, most patients using medical cannabis considered that this drug represents a better option than narcotics ie, opioids for adequate pain management. Additional studies on medical cannabis should evaluate whether the experience and perspective presented through this study could translate into satisfactory and consistent clinical outcomes. As a library, NLM provides access to scientific literature. Torres-Lugo, and Dr. Rivera-Dones and Dr. Find articles by Norberto J Torres-Lugo. Find articles by Alexandra Claudio-Marcano. Find articles by Luis Lojo-Sojo. Torres-Lugo: norberto. Published by Wolters Kluwer Health, Inc. Open in a new tab. Questions Yes No Do you think medical insurance should cover the cost of medical cannabis products in the future? Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel. Do you think medical insurance should cover the cost of medical cannabis products in the future? Do you think hospitals should allow or consider the use of cannabis products while being hospitalized? Do you think medical cannabis control pain more effectively than narcotics? Do you recommend the use of medical cannabis over other analgesics and medications?

Find Quality Weed in Gori: Your Local Guide

Gori buying ganja

Not a MyNAP member yet? Register for a free account to start saving and receiving special member only perks. Below is the uncorrected machine-read text of this chapter, intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text of each book. This is as true for marijuana as for tobacco. In both instances, smoke is drawn into the lungs where it can harm not only the cells that line the airways trachea, nasopharynx, bronchi, and alveoli and constitute the lung tissue, but also impair such cells as lung macrophages, which are part of the immune system. As a result, the smoke may inflict injury directly on parts of the system and also make the lungs vulnerable to agents that normally are held at bay by self-cleansing and self-protecting mechanisms. Different effects would be expected from tobacco and marijuana smoking because of the striking differences in the way in which the two substances are smoked: marijuana smoke usually is drawn deeply into the lungs by one or a few deliberately deep breaths, whereas tobacco smoking is generally more automatic, repetitive, and variable in pattern. Moreover, because marijuana is a 'street drug,' it not only is inconsistent in its content but also is subject to contamina- tion. Also, filters are not usually used by marijuana smokers, although water pipes are used occasionally. Consequently, under natural conditions it is difficult to judge dosage of active ingredients, to sort out the influence of contaminants, and to compare the consequences of marijuana and tobacco smoke. But, although cannabis products have been smoked for centuries, remarkably little is recorded about their effects on the lungs. Whatever contemporary information exists is confounded by the fact that most marijuana smokers are also tobacco smokers. In recent years, interest has heightened in the smoking of marijuana as a therapeutic measure. The inhalation route takes advantage of the large surface area afforded by the lungs for administering the effective constituents of marijuana. However, this In brief, our appraisal must assess the impact of chronic bronchial irritation and inflammation on the airways and gas-exchanging surfaces of the lungs. Acute Effects Marijuana affects the control of the breathing pattern in different ways depending upon the dose, the preparation, and its psychotropic effect on the consumer. On the other hand, larger doses of smoked marijuana may depress the ventilation and responsiveness to the CO2 stimulus Weil et al. The intravenous administration of ATHC in equivalent doses has much less of an effect either on the ventilation or on the effectiveness of CO2 as a respiratory stimulant Malit et al. Much more consistent and predictable is the effect of marijuana on the airways. The inhalation of small amounts of marijuana smoke causes bronchial dilation in persons without demonstrable lung disease Tashkin et al. The bronchodilation is easily demonstrable; the inhalation of isoproterenol l ug , a potent bronchodilator, caused less of an improvement in airways conductance than the peak effect observed after smoking 2 percent marijuana Tashkin et al. Ingestion of ATHC is less effective than smoking marijuana in producing bronchodilation; the bronchodilator effects of smoked marijuana last as long as 60 minutes; that of ingested ATHC up to 6 hours. Aerosolized ATHC has a local irritating effect on the airways, which often overrides the bronchodilating effect to the point of making it unsuitable for therapeutic purposes Tashkin et al. Except for bronchodilation, acute exposure to marijuana has little effect on breathing as measured by conventional pulmonary tests. Thus, in young marijuana smokers 2l years of age who smoked at least four cigarettes per week and no tobacco for at least 6 months before, ventilatory mechanics and gas exchange were normal by conventional tests Tashkin et al. In contrast, heavy marijuana smoking, i. Acute smoking of marijuana, as well as the ingestion of ATHC, also causes bronchodilation in individuals with mild to moderate asthma Tashkin et al. Marijuana smoking or ingestion of ATHC also dilated airways in asthmatics in whom bronchoconstriction was deliberately provided either by exercise or by the inhalation of methacholine, a bronchoconstrictor Shapiro et al. The mechanism by which bronchodilation is effected is not clear, but does not involve stimulation of beta-adrenergic. Adding to the difficulties of interpretation are the psychotropic effects of marijuana: four of the individuals who had previously used cannabis could distinguish the marijuana cigarette from the placebo on the basis of the intoxicating experience afforded by the marijuana smoke. Although the four subjects without previous cannabis experience did not experience any central nervous system effects, they did note mild somnolence or light-headedness after marijuana use. Among the experiments with induced asthma were some that employed the inhalation of cannabinoid-free marijuana smoke Tashkin et al. The results indicate that the smoke of the marijuana cigarette does not prevent methacholine-induced bronchospasm Tashkin et al. Smoking of marijuana did not aggravate or perpetuate bronchoconstriction in stable asthmatics, and it promptly reversed experimentally induced bronchospasm Tashkin et al. Addition of ATHC to placebo smoke caused a prompt, complete, and sustained reversal of methacholine-induced bronchospasm. Although ingestion of ATHC in a sesame oil vehicle has produced bronchodilation in asthmatic patients, less dilation was noted than after smaller doses of ATHC delivered by smoking Tashkin et al. Although it appears that the mechanism of ATHC-induced bronchial dilation is mediated by the autonomic nervous system, the process of dilation is not understood Gill and Paton, l; Cavero et al. Subacute Effects Pulmonary function tests in 28 healthy young experienced cannabis users before and after a day period of heavier than customary marijuana usage group daily average of 5. Cessation, by reduction in smoking, gradually restored the tests toward normal. The clinical significance of these abnormalities is uncertain. The marijuana smoked and the impairment in pulmonary function, coupled with the observation that reversibility of function was incomplete l week after marijuana smoking had stopped, suggests that heavy marijuana smoking over a much longer period could lead to clinically significant and less readily reversible impairment of pulmonary function. Chronic Effects A study of 3l American soldiers stationed in West Germany who smoked large quantities of hashish lOO grams or more per month for periods. In one-third of the soldiers, sputum-producing coughs, difficulty in breathing, and wheezing followed 3 to 4 months of regular use of hashish. However, they had a normal chest radiograph and normal sputum. Antibiotics failed to relieve the symptoms. The symptomatic patients could not work and four required hospitalization. An unspecified decrease in hashish consumption improved their symptoms. Pulmonary function tests in these individuals showed mild airway obstruction after 3 days of lessened hashish intake. Patch and serological tests failed to implicate allergy as a cause of the upper respiratory symptoms and signs. In Jamaica Hall, l , where marijuana usage is heavy, chronic bronchitis is frequent. However, marijuana smoking is usually associated with tobacco smoking, which confounds interpretation of the effects of marijuana alone. Adding to the uncertainty about the effects of marijuana as a cause of chronic regulatory abnormalities are two other studies, one in Jamaica Rubin and Comitas, l and the other in Costa Rica Hernandez-Bolanos et al. These results cannot be accepted as conclusive, because in each study the number of marijuana smokers was small, the subjects were not randomly selected, and the use of tobacco was not taken into account. Much more convincing is a recent study Tashkin et al. Care was taken to obtain proper control groups. The results indicated that habitual smoking of marijuana causes a mild but significant increase in resistance to airflow in the large airways without an appreciable effect on conventional tests. Another study was of American soldiers stationed in West Germany who voluntarily sought medical attention for such respiratory symptoms as pharyngitis, sinusitis, bronchitis, and asthma related to chronic heavy hashish smoking Henderson et al. Analysis of the hashish available and in use in the locale of this study showed concentrations of 5 to l0 percent ATHC. Two to 3 percent of samples were contaminated with cocaine, opium, morphine, spices, or feces. Two aspects of hashish smoking are relevant to the question of lung injury produced by hashish: l hashish is usually smoked in a pipe occasionally in a water pipe , although it is occasionally eaten, drunk as a tea, or rolled into a cigarette and smoked, and 2 hashish smoke generally is regarded by users as burning much hotter than tobacco smoke. Soldiers with pharyngitis usually smoked less than 25 grams of hashish monthly; those with bronchitis and asthma consumed more than 50 grams per month. The common complaint of sore throat in these. Persistent rhinitis inflammation of the nasal mucous membranes was present in 26 patients. As a rule, allergy could not be implicated in the nasopharyngeal manifestations. Treatment with antibiotics, decongestants, and phenylephrine a vasoconstrictor relieved the symptoms, but they recurred in those who continued smoking hashish. Chest radiographs were consistently normal, but pulmonary function was abnormal; the vital capacity the maximum volume of gas taken in was l5 to 40 percent below normal. In six of these subjects who smoked 50 or more grams per month, biopsy of bronchial mucosa revealed changes that resembled the abnormalities that occur in older heavy smokers of tobacco Auerbach et al. The biopsies also turned up atypical cells not found in tobacco smokers. The study of a respiratory disease in hashish or marijuana smokers is difficult because the great majority also smoke tobacco cigarettes. Also, the illegality of marijuana smoking prevents people from volunteering information and cooperating in experimental studies. Baseline physiological or clinical studies are difficult, because the subject is not identified until he seeks medical help. Rats Fleischman et al. At autopsy, the animals demonstrated damage of the airways and also of the lung substance. However, it is difficult to relate the results of these animal experiments, in which the artificial pattern of smoking differed markedly from that of the human smoker, to the effects that chronic marijuana smoking might elicit in man. Defense Mechanisms Alveolar Macrophages Little is known about the effects of marijuana on the defense mechanisms of the lungs. Although some observations have been made on the alveolar macrophage, an important element in this system, the results have been inconsistent. For example, some studies of the rat lung found that macrophages obtained by washing out the lung and exposing them to marijuana smoke manifested a depression in bactericidal activity Huber et al. On the other hand, another report failed to disclose a significant effect, not only of marijuana, but also of tobacco smoke on the bactericidal activity of macrophages Drath et al. Finally, others have found that alveolar macrophages differ slightly in their morphological responses to tobacco and to marijuana smoke. The significance of. Explants of lung have also been examined after exposure in culture to marijuana smoke Leuchtenberger et al. Striking changes have been observed in the appearance and growth characteristics of exposed cells. Carcinoma of the Lung The effect of marijuana as a carcinogen for lung, airways, and upper respiratory organs has not been systematically explored. Evaluating the carcinogenicity of marijuana is difficult, because most marijuana smokers also are tobacco cigarette smokers and because such carcinogenicity could have a long period of latency; studies of tobacco carcinogenesis indicate that 20 to 30 years of exposure must occur before tumors appear in the lung. It is understandable that information concerning the carcinogenic properties of marijuana are not yet available, particularly in the United States, where the agent has come into extensive use only during the past two decades. An important problem in evaluating carcinogenicity is the fact that the leaf is used by igniting it and the inhaled products of its combustion may be carcinogenic, as in the case of tobacco products. Even if it proved to be carcinogenic, the question would still remain as to what constituent in marijuana smoke was at fault. The potency of a substance as a mutagen ability to change genetic material can provide a clue as to its possible role as a carcinogen. Induction of genetic mutations by a substance in test strains of bacteria correlates with induction of tumors in test animals. Fractions from extracts of marijuana smoke particulates 'tar' have been found to produce dose-related mutations in four out of five test strains of bacteria Busch et al. The extent to which marijuana smoke differs from tobacco smoke is discussed in detail in Chapter l. In general, except for the presence of cannabinoids in one and tobacco alkaloids nicotine in the other, the combustion products of tobacco and marijuana are qualitatively similar. On occasion, however, differences that may be meaningful have been found. For example, one study Hoffmann et al. Tumorigenicity of marijuana and tobacco smoke condensates on mouse skin have been reported. In mice painted three times weekly with a tar suspension of smoke condensate, survival at 74 weeks was better in the marijuana group than in the tobacco group. Six of l00 mice painted with marijuana condensate developed skin tumors, all of which were benign, whereas l4 of l00 in the tobacco condensate group developed tumors, two of them malignant Hoffman et al. Exposure of human lung cells in culture to freshly generated marijuana smoke for up to 2 months resulted in increased mitotic indices, stimulation of ONA synthesis, and an increase in the population of cells with four times the DNA content of control cells or those exposed to tobacco smoke Leuchtenberger et al. Long-term exposure of hamster lung cells to the smoke of either marijuana or tobacco led to abnormal proliferation and malignant transformation within 3 to 6 months of exposure Leuchtenberger and Leuchtenberger, l Since malignant transformation was also noted in unexposed lung cells after l months of culture, it appears that the smoke of marijuana or tobacco accelerates, rather than initiates, the malignant change. Although no instance of human lung carcinoma attributable solely to marijuana smoking has yet been reported, abnormalities suggestive of cancerous lesions have been recorded. For example, in several of the U. In the hashish smokers who did not smoke tobacco, abnormalities in the tracheal biopsies were no more frequent or severe than in those persons who smoked only tobacco. Exception has been taken to the idea of an additive effect of tobacco and hashish smoke. A Greek study that compared chronic hashish and tobacco users with tobacco smoking controls found that although the hashish smokers had considerably more throat irritation and cough, the prevalence of bronchitis in both groups was about the same Boulougouris et al. The differences between the Greek and American studies may reflect differences between the two populations: The American study, done in Germany, favored inclusion of men with severe respiratory disturbances Tennant et al. However, evidence to support this hypothesis is not available. Because marijuana smoking is an ancient. Unfortunately, no reliable data have been gathered to settle this question. Heavy smoking of marijuana, in quantities comparable to that of tobacco, has been relatively uncommon in the United States. Therefore, the contribution of marijuana smoking to the incidence of primary lung cancer cannot yet be answered with any authoritative data. Summary: Respiratory System Lung Function and Defense Mechanisms The most important question about the effects of marijuana on the health of the respiratory system is whether acute or chronic marijuana smoking cause detectable structural or functional impairment of the lungs. Mild but measurable airway obstruction, affecting both large and small airways, can be shown to exist after 6 to 8 weeks of smoking marijuana daily, averaging five marijuana cigarettes a day; this decrement in function is reversible, but does not return to normal within one week of abstaining from smoking. In persons with histories of heavy smoking, particularly of hashish, chronic inflammatory changes are seen in the bronchi and uvula, often in association with chronic sinusitis. These manifesta- tions of upper respiratory disturbance have been described in individuals with histories of marijuana smoking usually in excess of 3 years and are reversible when marijuana smoking is stopped. Acute exposure of alveolar macrophages in vitro to marijuana smoke causes a reduction in phagocytic activity, a cell defense mechanism. The agents responsible for this change in macrophage function are in the vapor phase of marijuana smoke and are not related to the presence of ATHC. Also, lung explants exposed to marijuana smoke in vitro show changes in the chromosomal structure of nuclei. There is as yet no information about the effects of prolonged smoking of marijuana, that is, beyond 5 years. Particularly conspicuous is the lack of information about the effect of chronic marijuana smoking begun in late childhood or adolescence and continued to adulthood. Morphological changes associated with smoking marijuana could be compared with the morphological abnormalities associated with chronic tobacco smoking. The acute response to inhalation of marijuana is an appreciable bronchodilation, both in normal subjects and in individuals with. However, the bronchodilator effects of marijuana are a response to acute exposure; chronic exposure usually evokes bronchoconstriction. With respect to therapeutic application, the effects of smoking marijuana in producing bronchial dilatation do not exceed those that follow the inhalation of beta-agonist drugs. Moreover, the doses required for bronchodilatation usually elicit the psychotropic effects of marijuana and may be associated with changes in the structure of bronchial and parenchymal lung cells, the significance of which remains to be assessed. For these reasons therapeutic usefulness as a bronchodilator drug is open to serious question see Chapter 7. Carcinoma of the Lung One of the great uncertainties about marijuana smoking is its neoplastic potential. No reliable data are available concerning the incidence of carcinoma of the lungs and upper respiratory passages in long-term users of cannabis. Although this is not threatening to the normal heart, the rapid heart action can be harmful to the heart in which the circulation is compromised by atherosclerosis or is on the verge of failing. The responses of the cardiovascular system to acute exposure to marijuana differ between human beings and most other mammals in that the human subject typically responds with an increase in heart rate Bright et al. Human blood pressure usually increases moderately on acute administration of ATHC, but in monkeys and dogs acute administration is followed by a decrease in systemic arterial pressure. Typical effects on heart rate and blood pressure have been attributed to altered autonomic function Loewe, l; Joachimoglu, l; Ames, l; Gill and Paton, l Effects on the cardiovascular system are to some extent a function of dose, route of administration, and duration of exposure. Tolerance to some of the cardiovascular effects in human beings develops with chronic use Benowitz and Jones, l, la,b; Nowlan and Cohen, l , but continued use does not result in any persistent alteration in cardiovascular function after cessation of exposure Dornbush and Kokkevi, l Although part of the discrepancy may be attributable to differences in dosages, not all of it can be rationalized this way, leaving an unexplained disparity. Hemodynamic Effects Effects of marijuana on blood pressure and cardiac output, as mentioned above, are a function of the nature of exposure acute or chronic , of the dose, and of the body position; also, there are differences among human beings and a number of mammalian species. In human beings lying supine, acute exposure to ATHC typically causes a modest increase in blood pressure, although in some instances no significant change in pressure has been observed Beaconsfield et al. On assuming the upright posture, blood pressure may drop considerably. Cardiac output, in the supine position following an injection of ATHC, has been found to increase by as much as 30 percent Malit et al. The increase in cardiac output in the face of only a modest increase in blood pressure clearly results in a substantial decrease in peripheral vascular resistance. The change in resistance varies among the different vascular beds, being greatest in the vessels to the skeletal muscles. Chronic administration of quite large oral doses of ATHC exerts different effects than the acute on the circulation Bernstein et al. Systolic and diastolic pressure usually fall slightly, but these changes are not always sustained. As the blood pressure falls, the heart rate slows from the high levels caused by initial marijuana administration. The decrease in blood pressure can be accentuated if the subject assumes an upright posture. The extent to which it drops appears to be a reciprocal function of the extent to which plasma volume has increased. Changes in heart rate, afterload systemic vascular resistance, blood pressure , or preload plasma volume, venous return individually can cause changes in heart size and ventricular performance. In spite of these limitations, conclusions can be drawn from the observations on human beings. Definitive animal studies of ATHC effects on ventricular performance have not been done. Indices of cardiac performance usually improve after marijuana or ATHC. Almost invariably this improvement can be attributed to the increase in heart rate Gash et al. Beta-adrenergic blockade by propranolol is followed by less striking changes in the contraction time intervals. Another study of l7 subjects who smoked two to three cigarettes 20 mg ATHC per cigarette found cardiac output increased by 28 percent and heart rate by 30 percent, in conjunction with a slight decrease in stroke volume, which affects pulse pressure Tashkin et al. Autonomic Nervous System Marijuana could influence autonomic function in several ways: l by changing the sensitivity of reflexes that influence and control cardiovascular function; this effect could result either from changes in the processing of nerve impulses in the central nervous system or autonomic ganglia a group of nerve cells outside the central nervous system , from changes in the liberation or metabolism of transmitters at the autonomic nerve terminals, or from changes in the sensitivity of the pre- or postjunctional receptors; 2 by a change in the levels of neurotransmitters, the catecholamines norepinephrine, epinephrine in the blood as a result of actions on the adrenal medulla, which secretes these neurotransmitters; activation of the adrenals could be a direct effect or by reflexes or by a central action of ATHC; and 3 by exerting effects on dopamine activity an intermediate product in the synthesis of norepinephrine either in the central nervous system or periphery. Unfortunately, it is unclear how the effects of ATHC are exerted on the autonomic nervous system Truitt and Anderson, l97l; Beaconsfield et al. The data are insufficient to determine if the effects come by way of the central nervous system, or by peripheral neural structures, or by the adrenal medulla. It is also difficult to assess the role of. Finally; other possibilities, such as desensitization or blockade of peripheral adrenergic receptors, have not been examined. For example, ATHC appears to reduce a number of autonomic reflexes: After marijuana, the typical changes in heart rate and blood pressure elicited by the Valsalva maneuver a forced exhalation effort against the closed glottis are decreased, and so are the reflex circulatory responses to immersion of the hand in cold water Beaconsfield et al. However, during chronic administration of ATHC, no change occurs in the reflex decrease in heart rate caused by infusion of a dose of the vasoconstrictor phenylephrine sufficient to increase the blood pressure Benowitz and Jones, l; Benowitz et al. Smoking 20 mg of ATHC decreased the duration of exercise but caused no change in any cardiopulmonary parameter at any work load except for heart rate, which increased Shapiro et al. Chronic administration, on the other hand, has distinct effects. With chronic ingestion of large doses of ATHC there is a consistent gain in body weight and plasma volume, the latter caused by sodium retention Benowitz and Jones, l, la,b. The change in plasma volume seems to be causally related to the decrease in orthostatic hypotension during chronic exposure. The mechanisms responsible for the retention of salt and water have not been explored and may include changes in renal perfusion, inhibition of prostaglandin a substance that affects blood pressure synthesis by ATHC Burstein and Raz, l; Howes and Osgood, l , or some modification in pituitary-adrenal function Birmingham and Bartova, l Abnormal Heart and Circulation Although smoking marijuana or the introduction of ATHC into the body is apparently without deleterious effect on the normal heart and circulation, the possibility is great that the abnormal heart and circulation will not be as tolerant of an agent that speeds up the heart, sometimes unpredictably raises or drops the blood pressure,. Therefore, it is pertinent to examine the prospects that marijuana or ATHC may be harmful in individuals with coronary heart disease, cerebrovascular disease, hypertension, and heart failure. Moreover, it may be important to determine if ATHC interacts in its effects on the abnormal heart or circulation with other agents that are being administered for therapeutic purposes. Coronary Heart Disease Data on this topic are sparse, presumably because of the relatively short time that marijuana has been available in this country. Those who have smoked marijuana are just entering the age when coronary atherosclerosis is common. However, it has been shown both in normal individuals and in individuals with coronary artery disease that the acute administration of ATHC by smoking or injection can cause changes in the electrocardiogram ECG Johnson and Domino, l97l; Beaconsfield et al. Premature beats have also been noted. The reasons for the changes are unclear. Also not understood is the contribution of the increase in heart rate itself to the ECG changes and to the premature beats. In some patients with coronary artery disease, increased catecholamines can induce arrhythmias. It seems likely that in such patients ATHC could have the same effect. Also, in patients with coronary artery disease a large increase in heart rate can induce angina pain and even ischemic damage from insufficient oxygen as a result of an obstructed blood vessel. If ATHC were to increase heart rate markedly in such patients, and at the same time increase the need for cardiac perfusion because of the increased cardiac work and because of the intensified effect of catecholamines on the heart, it seems reasonable that there could be induction of angina and potentially precipitation of ischemic damage. Furthermore, if ATHC dulled the appreciation of pain and the appropriate responses to pain, the patient might not take suitable measure to relieve the angina, thereby increasing the risk of damage or arrhythmias. A decrease in oxygen-carrying capacity of blood because of formation of carboxyhemoglobin could also be troublesome. Exercise tolerance has been reported to decrease in individuals with angina after smoking marijuana; this decrease is in contrast to the unaffected exercise tolerance after smoking a placebo marijuana cigarette Aronow and Cassidy, l Oral ingestion of ATHC or smoking marijuana apparently can cause marked hypertension in association with an increase in systemic vascular resistance Benowitz et al. These observations concur in indicating that marijuana and ATHC increase the work of the heart, often in many ways. The conclusion seems inescapable that this increased work, coupled with stimulation by catecholamines, may tax the heart to the point of clinical hazard. In the occasional patient who develops hypertension after smoking, there would be an increased risk of a cerebral vascular accident stroke. Also, because ATHC administered after atropine can cause marked increases in blood pressure, this combination would place the patient with cerebro- vascular disease at risk, as would smoking after ingestion of other muscarinic blockers. In some patients, postural hypotension could be a problem, not only for persons with abnormal cerebral circulations, but also with abnormal coronary circulations. Hypertension The factors that act to intensify angina would be of importance in hypertensive patients. Although data are lacking on the magnitude of change in blood pressure caused by ATHC in hypertensives, it seems reasonable to assume that hypertensives smoking marijuana might have a greater increase in blood pressure than normals do. The increase in plasma volume and sodium retention that are associated with chronic exposure to ATHC could increase blood pressure in hypertensives and the mechanisms responsible for these changes very likely would interfere with the action of a number of antihypertensive medications. Heart Failure Because marijuana can cause tachycardia, a decrease in systemic vascular resistance required for increased cardiac output to sustain blood pressure and salt and water retention might place patients with severe heart failure at a disadvantage by exposure to ATHC. Data on such patients are lacking. In older patients treated by ATHC or who have smoked marijuana for glaucoma or cancer, orthostatic hypotension has been both disabling and a threat of cardiovascular complications Merritt et al. However, tolerance to orthostatic hypotension seems to develop during continued intake of ATHC or continued smoking of marijuana. Dehydration, as during vomiting or diuretic therapy, predisposes to the orthostatic hypotensive effects and resists the development of tolerance because it prevents expansion of blood volume. Interactions with Cardioactive Drugs Few studies evaluate interactions between ATHC and other drugs that act directly or indirectly on the heart. Propranolol usually attenuates the increase in heart rate caused by ATHC. A number of possible interactions can be imagined. If a patient were taking a drug that blocked uptake of catecholamines by nerve terminals, then those effects of ATHC that are mediated by catecholamines would be intensified. Because a great many psychotropic and antihypertensive drugs modify metabolism of neurotransmitters in the central nervous system and periphery, a wide variety of interactions with ATHC seems possible. Summary: Cardiovascular System The smoking of marijuana causes changes in the heart and circulation that are characteristic of stress. But there is no evidence to indicate that it exerts a permanently deleterious effect on the normal cardiovascular system. Neither is there convincing evidence that marijuana would be of particular benefit in treating any of the major forms of cardiovascular disease. The situation is quite different for those with an abnormal heart or circulation. Evidence abounds that marijuana increases the work of the heart, usually by increasing heart rate, and in some persons by increasing blood pressure. This increase in workload poses a threat to patients with hypertension, cerebrovascular disease, and coronary atherosclerosis. The magnitude and incidence of the threat remains to be determined because marijuana smoking has largely been confined to younger adults who are only now entering the age of serious complications of atherosclerosis on the heart, brain, and peripheral vessels. Marijuana also can cause postural hypotension. This drop in blood pressure could be hazardous in those individuals with compromised blood flow to the heart or brain, especially if they are volume-depleted dehydrated or if other drugs have impaired reflex control of their blood vessels. Marijuana appears to intensify the effects of the sympathetic nervous system on the heart, an undesirable consequence in patients with coronary artery disease and in those susceptible to arrhythmias. Many of the undesirable effects of marijuana on the cardiovascular system seem to become less severe following chronic exposure. Whether the relative paucity of reports of the ill-effects of marijuana on the abnormal cardiovascular system is a consequence of adaptation to chronic usage or to lack of exposure to marijuana of a population that is sufficiently advanced in years to be susceptible to its untoward effects remains to be determined. Recommendations for Research Additional studies are needed both l to provide information on the mechanisms responsible for the observed effects of marijuana on the cardiovascular system and 2 to provide new data on the effects of marijuana in patients with known forms of cardiovascular disease. Direct effects on the heart are not likely to differ among species, and thus experiments can be planned for a 'standard' heart preparation. For this purpose, it would be essential to use some vessels that did, and others that did not, have functioning nerve terminals. It would be important here to include studies on selected coronary vessels and on vessels which play a dominant role in the regulation of systemic vascular resistance. Additionally, studies should be done on the use of standard monitoring techniques to quantify any effect of marijuana smoking on tendencies toward arrhythmias, and on interactions of ATHC with drugs that modify synaptic transmission in the central nervous system. Vasoconstrictor actions of A and Atetrahydrocannabinol in the rat. Ames, F. A clinical and metabolic study of acute intoxication with cannabis sativa and its role in the model psychoses. Aronow, W. Effect of marihuana and placebo- marihuana smoking on angina pectoris. Auerbach, 0. Changes in bronchial epithelium relation to cigarette smoking and in relation to lung cancer. Marihuana smoking: Cardiovascular effects in man and possible mechanisms. Bellville, J. Respiratory effects of Atetrahydrocannabinol. Benowitz, N. Cardiovascular effects of prolonged Atetrahydrocannabinol ingestion. Effects of Atetrahydrocannabinol on drug distribution and metabolism. Prolonged Atetrahydrocannabinol ingestion: Effects of sympathomimetic amines and autonomic blockades. Cardiovascular effects of intravenous Atetrahydrocannabinol: Autonomic nervous mechanisms. Bernstein, J. Physiological assessments: Cardiopulmonary function, pp. In Mendelson, J. New York: Plenum Press, l Birmingham, M. Effects of cannabinol derivatives on blood pressure, body weight, pituitary-adrenal function, and mitochondrial respiration in the rat, pp. In Nahas, G. Marihuana: Chemistry, Biochemistry, and Cellular Effects. New York: Springer-Verlag, l Boulougouris, J. Effect of chronic hashish use on medical status in 44 users compared with 38 controls. Bright, T. Effects of beta-adrenergic blockade on marihuana-induced tachycardia, pp. Washington, D. Burstein, S. Prostaglandins , l Busch, F. Mutagenic activity of marihuana smoke condensates. Cancer Lett. Cavero, I. Parasympatholytic activity of - -deltatranstetrahydrocannabinol in mongrel dogs. Studies on the bradycardia induced by - -Atranstetrahydrocannabinol in anesthetized dogs. Dornbush, R. Acute effects of cannabis on cognitive, perceptual, and motor performance in chronic hashish users. Metabolic and functional characteristics of alveolar macrophages recovered from rats exposed to marijuana smoke. Englert, L. Fleischman, R. Pulmonary pathologic changes in rats exposed to marihuana smoke for l year. Gash, A. Effects of smoking marihuana on left ventricular performance and plasma norepinephrine: Studies in normal men. Gill, E. Pharmacological experiments in vitro on the active principles of cannabis, pp. In Joyce, C. The Botany and Chemistry of Cannabis, l Glatt, H. A-l-tetrahydro- cannabinol and l-alpha, 2-alpha-epoxyhexahydrocannabinol: Mutagenicity investigation in the Ames test. Graham, J. Cardiovascular and respiratory effects of cannabis in cat and rat. Hall, J. Government Printing Office, l Hardman, H. An overview of the cardiovascular- autonomic action of cannabis, pp. In Braude, M. Pharmacology of Marihuana. New York: Raven Press, l Henderson, R. Respiratory manifestations of hashish smoking. Hernandez-Bolanos, J. Preservation of pulmonary function in regular, heavy, long-term marijuana smokers. Ho, B. The effect of repeated administration of - -Atetrahydrocannabinol on the biosynthesis of brain amines. Sites of neurochemical action of Atetrahydrocannabinol: Interaction with reserpine, pp. Hoffmann, D. On the carcinogenicity of marijuana smoke, pp. In Runeckles, V. Howes, J. The effect of Atetrahydrocannabinol on the uptake and release of l4C-dopamine from crude striatal synaptosomal preparations. Neuropharmacology l3:lllll4, l Cannabinoids and the inhibition of prostaglandin synthesis, pp. Huber, G. Depressant effect of marihuana smoke on antibactericidal activity of pulmonary alveolar macrophages. Chest , l An experimental animal model for quantifying the biologic effects of marijuana on the defense system of the lung, pp. Marihuana: Biological Effects. Oxford: Pergamon Press, la. The gas phase of marijuana smoke and intrapulmonary bactericidal defenses. Marijuana, tetrahydrocannabinol, and pulmonary antibacterial defenses. Chest l0, l Huot, J. Cellular and biochemical alterations induced in vitro by delta-l-tetrahydrocannabinol: Effects on cell proliferation, nucleic acids, plasma cell membrane ATPase, and adenylate cyclase, pp. Joachimoglu, G. Natural and smoked hashish, pp. In Wolstenholme, G. Johnson, S. Some cardiovascular effects of marihuana smoking in normal volunteers. Kanakis, C. The effects of Atetrahydrocannabinol cannabis on cardiac performance with and without beta blockage. Circulation , l Kawasaki, H. Effects of Atetrahydrocannabinol on the cardiovascular system, and pressor and behavioral responses to brain stimulation in rats. Kochar, M. Electrocardiographic effects of marihuana. JAMA , l Leuchtenberger, C. Morphological and cytochemical effects of marijuana cigarette smoke on epithelioid cells of lung explants from mice. Nature , l97l. Effects of marijuana and tobacco smoke on human lung physiology. Nature 24l:ll39, la. Effects of marijuana and tobacco smoke on DNA and chromosomal complement in human lung explants. Nature , lb. Cytological and cytochemical studies of the effect of fresh marijuana cigarette smoke on growth and DNA metabolism of animal and human lung cultures, pp. Loewe, S. Pharmacological study, pp. Lancaster, Pa. Malit, L. Intravenous Atetrahydrocannabinol: Effects on ventilatory control and cardiovascular dynamics. Anesthesiology , l Martz, R. Propranolol antagonism of marihuana induced tachycardia. Life Sci. Merritt, J. Effect of marihuana on intraocular and blood pressure in glaucoma. Ophthalmology , l Nowlan, R. Tolerance to marijuana: Heart rate and subjective 'high. Perez-Reyes, M. Pharmacology of orally administered Atetrahydrocannabinol. Rosenkrantz, H. Acute, subacute and day chronic marihuana inhalation toxicities in the rat. Roy, P. Chronic inhalation of marijuana and tobacco in dogs: Pulmonary pathology. Rubin, V. The Hague: Mouton and Co. Seid, D. Pharmacologist 2l, l Shapiro, B. Mechanism of increased specific airway conductance with marijuana smoking in healthy young men. Effects of beta-adrenergic blockade and muscarinic stimulation upon cannabis bronchodilation, pp. New York: Raven Press, la. Cardiopulmonary effects of marijuana smoking during exercise. Chest l, lb. Stefanis, C. Biological aspects of cannabis use, pp. In Petersen, R. The National Challenge of Drug Abuse. HEW Publication No. ADM Sulkowski, A. Propranolol effects on acute marihuana intoxication in man. Psychopharmacology , l Acute pulmonary physiologic effects of smoked marijuana and oral Atetrahydrocannabinol in healthy young men. Tashkin, D. Acute effects of smoked marijuana and oral Atetrahydrocannabinol on specific airway conductance in asthmatic subjects. Effects of smoked marijuana in experimentally induced asthma. Subacute effects of heavy marijuana smoking pulmonary function in healthy young males. Bronchial effects of aerosolized tetrahydrocannabinol in healthy and asthmatic subjects. Short-term effects of smoked marihuana on left ventricular function in man. Chest , lb. Cannabis, l Respiratory status of seventy-four habitual marijuana smokers. Tennant, F. Medical manifestations associated with hashish. JAMA 2l6:ll, l97l. Histopathologic and clinical abnormalities of the respiratory system in chronic hashish smokers. Substance and Alcohol Misuse ll00, l Truitt, E. Biogenic amine alterations produced in the brain by tetrahydrocannabinols and their metabolites. Vachon, L. Single-dose effect of marihuana smoke: Bronchial dynamics and respiratory-center sensitivity in normal subjects. Experientia , l Vollmer, R. Role of the central automatic nervous system in the hypotension and bradycardia induced by - -Atrans-tetrahydrocannabinol. Wehner, F. Weil, A. Clinical and psychological effects of marihuana in man. Science lll, l Cardiovascular effects of Atetrahydrocannabinol in man. Zwillich, C. The effects of smoked marijuana on metabolism and respiratory control. Based on feedback from you, our users, we've made some improvements that make it easier than ever to read thousands of publications on our website. Jump up to the previous page or down to the next one. Also, you can type in a page number and press Enter to go directly to that page in the book. To search the entire text of this book, type in your search term here and press Enter. Ready to take your reading offline? Click here to buy this book in print or download it as a free PDF, if available. Do you enjoy reading reports from the Academies online for free? Sign up for email notifications and we'll let you know about new publications in your areas of interest when they're released. Get This Book. Unfortunately, this book can't be printed from the OpenBook. If you need to print pages from this book, we recommend downloading it as a PDF. Visit NAP. Looking for other ways to read this? No thanks. Marijuana and Health. Page 58 Share Cite. Page 59 Share Cite. Page 60 Share Cite. Page 61 Share Cite. Page 62 Share Cite. Page 63 Share Cite. Page 64 Share Cite. Page 65 Share Cite. Page 66 Share Cite. Page 67 Share Cite. Page 68 Share Cite. Page 69 Share Cite. Page 70 Share Cite. Page 71 Share Cite. Page 72 Share Cite. Page 73 Share Cite. Page 74 Share Cite. Page 75 Share Cite. Page 76 Share Cite. Page 77 Share Cite. Page 78 Share Cite. Page 79 Share Cite. However, this 57 58 practice entails the disadvantage of administering a therapeutic agent in a cloud of air pollutants. The mechanism by which bronchodilation is effected is not clear, but does not involve stimulation of beta-adrenergic 59 receptors or blockade of muscarinic receptors in airway smooth muscle Shapiro et al. Chronic Effects A study of 3l American soldiers stationed in West Germany who smoked large quantities of hashish lOO grams or more per month for periods 60 of 6 to l5 months found their ailments to be principally respiratory, including bronchitis, sinusitis, asthma, and rhinopharyngitis inflammation of the nasopharynx Tennant et al. The significance of 62 these differences, especially in terms of their long-term effect on pulmonary defense mechanisms, remains to be defined. Because marijuana smoking is an ancient 64 custom in Asia and the Middle East, lung cancer would be expected to be more prevalent in these parts of the world if a causal relationship did exist. It is also difficult to assess the role of 69 reflex adjustments in the heart and systemic circulation. Abnormal Heart and Circulation Although smoking marijuana or the introduction of ATHC into the body is apparently without deleterious effect on the normal heart and circulation, the possibility is great that the abnormal heart and circulation will not be as tolerant of an agent that speeds up the heart, sometimes unpredictably raises or drops the blood pressure, 70 and modifies the activities of the autonomic nervous system. Atropine 72 can greatly potentiate the ability of ATHC to increase systemic arterial pressure Benowitz and Jones, la,b. Login or Register to save! Stay Connected!

Gori buying ganja