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Official websites use. Share sensitive information only on official, secure websites. Rotterdam, The Netherlands. Email: h. The Hague, The Netherlands. Email: ajvanvelzen hotmail. Study visits were separated by 1 month, in which 1 of the study nebulizers was used twice daily. Tobramycin PK for both nebulizers was established using measured tobramycin concentrations and Bayesian PK modelling software. Hearing and renal function tests were performed to test for aminoglycoside associated toxicity. Patient and nebulizer satisfaction were assessed. Inhalations were well tolerated and serum trough concentrations below the predefined toxic limit were reached with no significant differences in PK parameters between nebulizers. Results of audiometry and estimated glomerular filtration rate revealed no abnormalities. Keywords: children, Cystic fibrosis, inhaled antibiotics, mesh nebulizer, pharmacokinetics. Survival of patients with cystic fibrosis CF has improved considerably over recent decades, because of better and new treatments including the use of nebulized antipseudomonal antibiotics. Therefore, treatment compliance and quality of inhalation are often low 4 and this may impair the beneficial effects of therapy. Moreover, standard nebulizer therapy is very inefficient. More convenient alternatives have been introduced in recent years, such as tobramycin inhalation powder and mesh or smart nebulizers. Full informed written consent was obtained from all patients aged 12 years and older and from both parents or legal representatives of all patients. The primary endpoint was systemic bioavailability of inhaled tobramycin, defined as serum tobramycin area under the concentration—time curve from 0 to 24 hours AUC 0—24h following a supervised inhalation with both nebulizers on separate days. Study duration for each patient was 1 month and consisted of 2 study visits at the CF centre. Patients were randomly assigned to treatment arm A or B. Blood samples for tobramycin analysis were collected predose and up to 24 hours postnebulization and no second dose was inhaled during this period. Randomization was stratified for age 6—11 and 12—18 years and centre randomized block design. During the visits blood, urine, and sputum or throat swab samples were collected, spirometry and hearing tests were performed and questionnaires were filled out by the children or their parents. Degree of symptoms regarding cough, sputum production, exercise tolerance, fatigue and disturbed sleep was also scored. Test protocols were equalized as much as possible for the 3 participating CF centres regarding equipment and analysis. Following inclusion of patient 14, a protocol amendment was written. Since patients still performed a supervised inhalation with both nebulizers, the primary endpoint of the study did not change. The nebulizer was filled with 4 mL Bramitob and patients inhaled until sputtering of the device, according to the manufacturer information. Patients inhaled until the device indicated that the full dose was administered. Since there were no medication chambers of 1 mL commercially available, patients inhaled 0. The remaining 3 mL of each ampoule was thrown away and not used for further administrations. No active compounds were inhaled during these training sessions. During the study visits, patients performed a supervised inhalation with the allocated nebulizer. No additional inhalations during this day were performed to allow for PK measurements during 24 hours. The second study visit was scheduled within 1—3 days of the last home inhalation. Samples were collected by patients themselves at home 3, 6 and 24 hours after inhalation. The following parameters were calculated: area under the concentration—time curve from 0 to 24 hours AUC 0—24h as measure for exposure, maximum serum concentration C max , serum concentration 12 and 24 hours after nebulization C trough and time to C max T max. Secondary endpoints included: differences in AUC 0—24h between age groups 6—11 and 12—18 years pharmacokinetics ; trough concentrations, change in renal and hearing function after 1 month inhalation and change in forced expiratory volume in the first second FEV 1 before and after supervised inhalations safety ; quality of life, adverse events, tolerability, nebulization time and nebulizer satisfaction patient satisfaction. For an extensive method description about the secondary endpoints, see Appendix S1. Estimated glomerular filtration rate based on serum creatinine eGFR is the standard clinical measure to assess and monitor renal function. Statistical analysis was performed with SPSS version The guideline on the investigation of bioequivalence 19 from the committee for medicinal products for human use was used to provide a statement about the bioequivalence of TIS nebulization between the 2 nebulizers. In accordance with this guideline, C max and AUC 0—24h were compared using a general linear model in order to assess equivalence. All patients completed PK data collection for both nebulizers. Table 1 reports patient characteristics baseline values visit 1. There were no significant differences in renal or lung function between study visits. Patient characteristics were comparable for the 2 treatment arms. Patients also had similar degree of symptoms regarding cough, sputum production, exercise tolerance, fatigue and disturbed sleep at visits 1 and 2. Both patients were included in the PK analysis, as well as in the evaluation of systemic toxicity and bronchospasm following the supervised inhalations and patient satisfaction. Serum concentration—time profiles are shown in Figure 1 see Supplementary Table S1 for details. Time to maximum serum concentration T max following tobramycin inhalation solution nebulization, reported per age group. No significant interaction effects between study visit day and nebulizer or between age group and nebulizer were found. Results of audiometry and eGFR revealed no abnormalities. For full results of the secondary endpoints, see Appendix S2. Data are presented as median range. Differences between nebulizers were not significant. Overall, there were no clear clinical signs of toxicity after 1 month of TIS inhalation with either nebulizer. The primary endpoint was systemic bioavailability of inhaled tobramycin, defined as serum tobramycin AUC 0—24h. No significant difference between nebulizers for this endpoint was found, nor for other PK parameters, and serum concentrations were in accordance with previously reported values. Subgroup analysis revealed no differences in PK parameters between age groups except for T max , for which possible explanations can be appointed. Since subgroups were small and variability was large, clinical relevance of this finding is however uncertain and no firm conclusions can be drawn. From the beginning of nebulization there is absorption and clearance and when 6 minutes is subtracted from the mean T max , there is no significant difference. A possible explanation could be delayed absorption due to increased mucus plugging in older children. Variability in systemic exposure of inhaled antibiotics is known to be large in CF patients and was also considerable in our study. Heterogeneity in disease severity and renal function, but also age, weight and variable competence in inhalation technique of the child may contribute to this variability. Interestingly, similar coefficients of variation were calculated for the nebulizers. However, no clear toxic limits have been defined yet for tobramycin during chronic inhalation. Consequently, reliable comparison between nebulizers regarding safety could not be made, though results seemed to be similar. Aminoglycosides have a cochleotoxic effect and can cause irreversible hearing loss. Audiometry results showed no abnormalities for most patients, which is in accordance with results from other studies regarding TIS safety. The eGFR values were similar for both study visits and nebulizer groups, indicating no clinical toxic effect on the kidneys. However, in all studies, variability was large and differences in nebulizer and dosing regimens hampers comparison between studies. Unfortunately, no other inhalation studies are available to compare our data with and the clinical relevance of the result cannot be assessed. As expected, the fold increase in our inhalation study is somewhat lower compared to the reported 3. Results from previous studies with intravenous aminoglycosides suggest that NAG values effectively return to pretreatment concentrations within 2—8 weeks after the end of therapy. The clinical relevance of this finding is currently unknown and requires further investigation, but the findings confirm the need for regularly monitoring of renal function while a child is on chronic inhaled tobramycin. However, in patients who frequently suffer from acute exacerbations or whose lung function deteriorates rapidly, a regimen of continuously inhaled tobramycin is sometimes used. Combined with an expected learning curve in the home treatment period, this could explain the higher nebulization time during the study visit. There are several limitations to address. There is a wide degree of variation in our PK results, although this degree of variability is not unusual for inhaled drugs and is inherent to the individual inhalation technique. Furthermore, the study was not powered for the secondary aim: the safety data. Also, because of the lack of serum sampling at day 28, possible accumulation following a regular treatment period could not be assessed. Moreover, only systemic exposure and no tobramycin airway concentrations or direct lung deposition were measured and clinical efficacy outcomes were not assessed in this study. We did perform Pa culture in sputum or throat swab samples in order to assess the success rate for eradication patients. Therefore, this study stresses the need for carefully monitoring for toxic effects of aminoglycosides in patients on chronic TIS therapy, especially when new nebulizers are used. All other authors: no competing interests to declare. The data that support the findings of this study are available from the corresponding author upon reasonable request. Table S1 Pharmacokinetic parameters following tobramycin inhalation solution nebulization. We thank all patients and their parents for their participation in this study. We would also like to thank the NCFS Dutch CF foundation for providing a research grant and Chiesi and Mediq Romedic for their support with the study medication and nebulizers, respectively. The study was partly funded by the NCFS. This foundation was not involved in the study design, acquisition, analysis and interpretation of data, or writing of the manuscript. Br J Clin Pharmacol. The authors confirm that the PI for this paper is Dr H. Janssens, MD, PhD, and that she had direct clinical responsibility for patients. This section collects any data citations, data availability statements, or supplementary materials included in this article. As a library, NLM provides access to scientific literature. Find articles by Annelies J van Velzen. Find articles by Joris WF Uges. Find articles by Harry GM Heijerman. Find articles by Bert GM Arets. Find articles by Marianne Nuijsink. Find articles by Erik M van Maarseveen. Find articles by Gijsbert A van Zanten. Find articles by Bas Pullens. Find articles by Daan J Touw. Find articles by Hettie M Janssens. Open in a new tab. Differences between treatment arms were not significant. Click here for additional data file. 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. Male a. Height cm b. Weight kg b. BMI b. Patients on maintenance TIS a. Tolerability scale 0—10 a. Coughing during nebulization. Coughing after nebulization. Dyspnoea during nebulization. Dyspnoea after nebulization. Dizziness during nebulization. Dizziness after nebulization. Study visits b. Home treatment period. Nebulizer satisfaction scale 0—10 c.

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Learning objectives and disclosure and ordering information can be found in the CME section at the front of this issue. Submitted for publication March 25, Accepted for publication May 9, Published online first on July 4, Corrected on October 18, Opioids are effective analgesics, but they can have harmful adverse effects, such as addiction and potentially fatal respiratory depression. Naloxone is currently the only available treatment for reversing the negative effects of opioids, including respiratory depression. However, the effectiveness of naloxone, particularly after an opioid overdose, varies depending on the pharmacokinetics and the pharmacodynamics of the opioid that was overdosed. In this review, the authors examine the pharmacology of naloxone and its safety and limitations in reversing opioid-induced respiratory depression under different circumstances, including its ability to prevent cardiac arrest. Naloxone, N -allylnoroxymorphone fig. It was first synthesized in and further developed through the early s in a successful effort to find a strong narcotic antagonist without negative side effects. Chemical structures of four opioids: morphine A , nalorphine B , oxymorphone C , and naloxone D. Naloxon was originally available for injection by intravenous, subcutaneous or intramuscular routes of administration. More recently, the U. Food and Drug Administration Silver Spring, Maryland approved intramuscular autoinjectors and intranasal naloxone, including over-the-counter intranasal naloxone, for treatment of opioid overdose and opioid use disorder. In recent years, knowledge on the pharmacokinetic and pharmacodynamic properties of naloxone has increased, and various limitations in its practical use were identified. For example, there are a series of conditions in which the effectiveness of naloxone as an opioid reversal agent is limited. These are predominantly related to the findings that the speed and magnitude of opioid reversal is dictated by opioid receptor association and dissociation kinetics, defined by rate constants K ON and K OFF , respectively, with limitations in reversal when K OFF values are low, causing difficulty in dissociating the opioid from its receptor. Opioids are highly effective analgesics, but their use is accompanied by undesirable side effects that include dependence and potentially lethal respiratory depression. These two side effects are a particularly lethal combination, which contributed to the current opioid crisis in the United States, Canada, and certain European countries, and are responsible for hundreds of daily opioid deaths. Depending on the condition of the patient, rescue may include cardiopulmonary resuscitation chest compressions , artificial ventilation mouth-to-mouth resuscitation, mask ventilation or intubation and assisted ventilation , and administration of opioid antagonists, most commonly naloxone. The success of rescue depends on many factors such as opioid dose, degree of opioid tolerance, the opioid affinity at the opioid receptor, cointoxication, comorbidities, timing of rescue, and experience of rescuers, among others. In most cases, naloxone is administered to improve or restore spontaneous breathing and prevent the sequence leading to a circulatory arrest. Note that the pathophysiology, patient demographics, and management of an opioid-induced cardiac arrest differ from those of an ischemic arrest related to an atherosclerotic plaque rupture. However, there are suggestions that in the event of a cardiac arrest, use of naloxone during a standard resuscitation including assisted ventilation is of limited benefit, and standard resuscitation medication suffices for restoration of cardiac activity. The many deaths from opioids indicate that rescue from respiratory depression is often ineffective or too late or not initiated. Interestingly, survival after an opioid-related out-of-hospital cardiac arrest is greater than after an arrest from other causes, indicating that those that overdose on an opioid are more resilient and younger with less comorbidities than other populations experiencing a cardiac arrest, although misdiagnosis in some cases cannot be excluded. This review will examine the pharmacology of naloxone and its effectiveness and limitations in reversing opioid-induced respiratory depression under various conditions. We will also discuss its ability to prevent cardiac arrest and briefly mention potential naloxone alternatives. Given its poor absorption and high metabolic breakdown, naloxone is not suitable for sublingual or oral administration. Still, also for the other administration routes, relatively high doses are needed to rapidly reach effective central concentrations after administration. Naloxone is primarily metabolized in the liver, while about one third of the dose is excreted unchanged via the kidney. In the liver, naloxone is glucuronidated into the inactive compound naloxoneglucuronide and to a minor extent metabolized by N -dealkylation and 6-oxo group reduction. In several studies in healthy young participants, we performed population pharmacokinetic model analyses of naloxone using two compartment models. Typical model parameter estimates were an elimination clearance of 3. At effective doses, naloxone will reverse the opioid effects, and consequently will cause loss of analgesia and respiratory depression and at a high dose may precipitate withdrawal symptoms in chronic opioid users. Its affinity for the different opioid receptors varies with affinity constants Ki approximately 1. The magnitude and speed at which naloxone reverses an opioid overdose depend on factors that are related to the opioid that requires reversal. So, naloxone effectiveness differs under varying conditions. Volpe et al. Relevant K OFF values are naloxone 0. We here give several specific naloxone reversal scenarios that depend on the circumstances that warrant reversal, such as 1 an opioid overdose in the perioperative setting, 2 and 3 the community setting in which fentanyl or a high-affinity opioid is overdosed, 4 the reversal of an opioid partial agonist, 5 reversal in case of a cointoxication with a tranquilizer, and 6 reversal in case of brain hypoxia. We refrain from discussing accidental exposure to fentanyl by skin contact or accidental inhalation of fentanyl powder, 21 or treatment of mass casualties from intentional release of aerosolized high-affinity opioids in the environment. In clinical practice, particularly at the end of surgery, opioid concentrations at the receptor are often just above the threshold for neuronal depression with consequently an absence of respiratory rhythmic activity. An intravenous route in the clinical setting is preferred above other routes of administration, as perioperative patients all have an intravenous access line. Since respiratory effect occurs at a higher receptor occupancy than analgesia, 5 this approach will have a limited effect on pain relief up to intravenous naloxone doses of 0. For example, intravenous naloxone doses of 0. In case of a fentanyl overdose in the community setting, an intravenous access line is unavailable and other routes of naloxone administration are used, such as intranasal or intramuscular routes. In a modeling study, Moss et al. Higher opioid dose or, more importantly, higher opioid concentrations in the brain complicate reversal, and standard reversal doses of intravenous naloxone 0. One has to be aware that after a single high naloxone dose, renarcotization still might occur. High-affinity opioids with slow receptor dissociation kinetics are used in clinical practice and often found in illegal substances. Again, also in this scenario, intranasal and intramuscular routes of naloxone administration are preferred due to lack of an intravenous access line. For optimal management of overdose-related respiratory depression, it is theoretically relevant to know the overdosed opioid K OFF value. However, for all practical purposes, it is best to assume slow receptor kinetics. This is particularly true since one can assume that the overdose is related to a high opioid dose with a prolonged duration of action, and the second limiting factor of naloxone effectiveness is its short duration of action. In case of any of these limiting events, high-dose naloxone or a continuous naloxone infusion is required for reversal. This was earlier demonstrated for buprenorphine, an opioid with high receptor affinity and a low K OFF value. Since continuous intravenous naloxone infusions are only possible under controlled conditions, alternatives have been developed such as intranasal or intramuscular naloxone, or long-acting naloxone analogs. Moreover, the rate or speed of reversal cannot be efficiently increased by increasing the naloxone dose fig. In a binding study, 27 Kang et al. These data are relevant as they exemplify the rapid return of opioid effect after naloxone treatment. Still, full reversal of respiratory depression is not necessary to sustain or reinitiate gas exchange in the lungs. Effect of naloxone dose A and effect of different receptor dissociation rate constant B on opioid-induced respiratory depression. Purple and orange arrows , Injection of the opioid; black arrow , injection of a single naloxone dose. B , The smaller the opioid K OFF , the increase in ventilation after a similar naloxone dose is less. Note that at low K OFF values, the degree of respiratory depression increases at a similar opioid dose. Data from Martini et al. Each dot is a 1-min average of the measured end-tidal carbon dioxide partial pressure. Data from van Lemmen et al. This results in a bell-shaped or inverse U-shaped naloxone dose-response curve rather than the expected sigmoid E MAX dose response with full reversal at increasing naloxone doses. The mechanism of the bell-shaped curve remains unknown, but possibly at high dose, the naloxone affinity for the receptor decreases causes loss of reversal effectiveness. Further studies are needed to improve our understanding of the naloxone—buprenorphine interaction. In many individuals that overdosed on an opioid, postmortem examination revealed that intoxication was due to multiple drugs. We earlier demonstrated that oxycodone-induced respiratory depression is enhanced by coadministration of ethanol, or the antidepressants paroxetine or tianeptine. The nonopioid may similarly be a potent respiratory depressant e. A potential alternative would be to combine naloxone with a nonopioid or agnostic respiratory stimulant or, in case of a benzodiazepine cointoxication, with the benzodiazepine receptor antagonist flumazenil. The inability to reverse the opioid effect when given in conjunction with gabapentinoids is exemplified is two rodent studies. These studies examined the effect of naloxone effectiveness in reversing opioid effect when combined with pregabalin or gabapentin. However, after pretreatment with either pregabalin or gabapentin, the dose was less effective, and a dose of 0. Since the gabapentinoids were devoid of respiratory depressant effect, these data suggest that the gabapentinoids affect increase the naloxone K OFF value. Probably the central depressant effects of hypoxia prevent reversal of respiratory rhythmic neuronal activity. These observations have evident clinical implications as any antidote, naloxone as well as agnostic respiratory stimulants, will be ineffective in case of severe hypoxia. This highlights the importance of ventilatory support in addition to naloxone administration in the case of a rescue attempt of an overdose victim. Cardiac arrest may occur after an opioid overdose due to apnea- or hypoventilation-induced asphyxia complicated by cardiac dysrhythmias. Mann et al. In fact, their model is the first to simulate the opioid overdosing with fentanyl and its congeners in the community setting. They describe the effects of low- and high-dose intravenous fentanyl 1. Their results are summarized as follows fig. A Simulations of the effect of intramuscular naloxone injection on minute ventilation top row , arterial oxygen partial pressure middle row , and cardiac output bottom row. Two opioids fentanyl and carfentanil and two doses per opioid are simulated. B Population simulations of the percentage of simulated individuals that experienced cardiac arrest under the simulated conditions given in A. Data from Mann et al. These simulations depict the sequence of events that lead to cardiac arrest and exemplify that the success of a naloxone intervention is dependent on opioid receptor kinetics, opioid dose and naloxone dose and concentration. What remains to study is to determine the influence of timing of the naloxone intervention on the success of rescue and prevention of brain damage and, equally important, to go beyond the current simulations and determine the influence of resuscitation on rescue after cardiac arrest occurred. Naloxone is a safe drug in the sense that when administered to healthy awake and opioid-naive individuals, it is generally without effect or side effects. Kagawa et al. In the event of an opioid overdose, naloxone may have adverse effects, albeit clinical data indicate that serious events are rare. Vasoconstriction and an increase in blood pressure and the occurrence of tachyarrhythmias may be the basis of these complications, with pulmonary edema arising from a rapid fluid shift or from inspiration against a closed glottis negative pressure pulmonary edema. Nalmefene is an opioid receptor antagonist that was earlier available in the United States for treatment of an opioid overdose, 47 and was not withdrawn from the market for reasons of safety or effectiveness, but because of commercial reasons. Since naloxone is not effective in a variety of overdose conditions, so-called agnostic respiratory stimulants are being developed. These stimulants allow reversal of respiratory depression without any interaction with the underlying cause of respiratory depression. We recently discussed a series of old and new nonopioid stimulants see van der Schrier 8 and references cited therein. Respiratory stimulants with promising results in animal or human studies include nicotinic acetylcholine receptor agonists, ampakines, potassium channel blockers, partial opioid receptor agonists or antagonists, scrubber molecules, and monoclonal antibodies against specific opioids including antibodies that enhance opioid metabolism. For example, it remains unknown whether these strategies are able to overcome severe respiratory depression e. In fact, we contend that most strategies share some of the naloxone drawbacks, and reversal might be difficult as we predict that under conditions of cardiorespiratory collapse, insufficient drug will reach the brainstem. Stimulants with a site of action outside the brain compartment might have an advantage such as potassium channel blockers that act at the carotid bodies , or there might be an advantage of combining any of these stimulants with naloxone to target two independent mechanisms with a possible better outcome than either treatment alone. The combinations of any of these stimulants with naloxone has been studied only sparsely. We gave an example above of the combination of low-dose naloxone and the nicotinic acetylcholine receptor partial agonist, varenicline. Such therapy evidently only works provided presence of circulation. Just one other study investigated treatment combined with an opioid receptor antagonist. In individuals with an opioid use disorder, the combination of a vaccine against oxycodone with prolonged-release naltrexone was more efficacious than either treatment alone in the prevention of oxycodone-induced respiratory depression. One disadvantage of agnostic stimulants has not received any attention as yet. Miner et al. Given the above, we encourage further studies on the combination of an agnostic respiratory stimulant with naloxone under conditions of acute respiratory depression, mimicking an overdose from synthetic opioids. However, its effectiveness is limited and determined by a variety of factors that interact in a complex fashion and remain poorly studied. Factors that that limit a rapid and full reversal may be divided into factors that relate to the opioid that has been overdosed and to the pharmacologic properties of naloxone. The latter factor is particularly relevant as a late attempt to rescue the patient may be complicated by a cardiac arrest. Given that most of these limitations remain unknown under real-life conditions, the optimal naloxone rescue dose remains uncertain, and current guidelines are based on simulation studies or retrospective case series. However, the utility of staggered naloxone administration after such a schedule has not been evaluated outside of controlled settings. Recognizing that typical clinical studies in overdose patients are not feasible, we advocate for robust and well-controlled pharmacokinetic and pharmacodynamic evaluations in relevant patient populations to allow development of well-informed guidelines for treatment of an opioid overdose in the community. Importantly, irrespective of the results of studies on single intoxications, one needs to be aware that proper reversal of polysubstance abuse and overdoses requires a different approach that might involve the combination of naloxone with an agnostic respiratory stimulant. Discussion of such compounds e. In the last 36 months, Dr. Dahan received consultancy fees from Enalare Therapeutics Inc. Princeton, New Jersey , Trevena Inc. Dahan holds Enalare stock options. The other authors declare no competing interests. Sign In or Create an Account. Search Dropdown Menu. Advanced Search. Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume , Issue 3. Previous Article Next Article. Naloxone, a Narcotic Antagonist. Naloxone Pharmacokinetics and Pharmacodynamics. Receptor Kinetics. Naloxone Ability to Prevent Cardiac Arrest. Naloxone Safety. Naloxone Alternative: Nalmefene. Naloxone Alternatives: Agnostic Respiratory Stimulants. Article Navigation. Education September Maarten van Lemmen, B. This Site. Google Scholar. Jeffrey Florian, Ph. Zhihua Li, Ph. Monique van Velzen, Ph. Eveline van Dorp, M. Marieke Niesters, M. Elise Sarton, M. Erik Olofsen, Ph. Rutger van der Schrier, M. David G. Strauss, M. Albert Dahan, M. Author and Article Information. Address correspondence to Dr. Anesthesiology September , Vol. Connected Content. Letter: Naloxone for Opioid Overdose: Reply. Letter: Naloxone for Opioid Overdose: Comment. Get Permissions. View large Download slide. Table 1. View large. View Large. Search ADS. Potency, duration of action and pA 2 in man of intravenous naloxone measured by reversal of morphine-depressed respiration. Incidence, reversal and prevention of opioid-induced respiratory depression. Development of a translational model to assess the impact of opioid overdose and naloxone dosing on respiratory depression and cardiac arrest. Combining opioids with benzodiazepines: Effects on mortality and severe adverse respiratory events. Advances in reversal strategies of opioid-induced respiratory depression. Differential impact of two critical respiratory centres in opioid-induced respiratory depression in awake mice. Dual mechanisms of opioid-induced respiratory depression in the inspiratory rhythm-generating network. Opioid-associated out-of-hospital cardiac arrest: distinctive clinical features and implications for health care and public responses: A scientific statement from the American Heart Association. Population pharmacokinetics of intravenous, intramuscular, and intranasal naloxone in healthy volunteers. Naloxone reversal of morphine- and morphineglucuronide-induced respiratory depression in humans. High-dose naloxone, an experimental tool uncovering latent sensitisation: Pharmacokinetics in humans. Uniform assessment and ranking of opioid Mu receptor binding constants for selected opioid drugs. Pharmacokinetic-pharmacodynamic modelling in acute and chronic pain: An overview of the literature. Higher naloxone dosing in a quantitative systems pharmacology model that predicts naloxone-fentanyl competition at the opioid mu receptor level. Opioid antagonism in humans: A primer on optimal dose and central mu-opioid receptor blockade. Modeling buprenorphine reduction of fentanyl-induced respiratory depression. Influence of ethanol on oxycodone-induced respiratory depression: A dose-escalating study in young and elderly volunteers. Effect of paroxetine or quetiapine combined with oxycodone vs oxycodone alone on ventilation during hypercapnia: A randomized clinical trial. Respiratory effects of the atypical tricyclic antidepressant tianeptine in human models of opioid-induced respiratory depression. Countering opioid-induced respiratory depression in male rats with nicotinic acetylcholine receptor partial agonists varenicline and ABT Gabapentin action and interaction on the antinociceptive effect of morphine on visceral pain in mice. Effect of gabapentinoids on heroin-induced ventilatory depression and reversal by naloxone. Morphineglucuronide: Analgesic effects and receptor binding profile in rats. Severe hypoxemia prevents spontaneous and naloxone-induced breathing recovery after fentanyl-overdose in awake and sedated rats. No effect of naloxone on hypoxia-induced ventilatory depression in adults. Acute opioid withdrawal following intramuscular administration of naloxone 1. Prehospital naloxone and emergency department adverse events: A dose-dependent relationship. Naloxone-associated pulmonary edema following recreational opioid overdose. Accessed March 24, Nalmefene in the treatment of internet pornography addiction — A case report and review of the literature. Fighting fire with fire: Development of intranasal nalmefene to treat synthetic opioid overdose. Effect of different absorption enhancers on nasal absorption of nalmefene hydrochloride. Combining a candidate vaccine for opioid use disorders with extended-release naltrexone increases protection against oxycodone-induced behavioral effects and toxicity. Noradrenergic mechanisms in fentanyl-mediated rapid death explain failure of naloxone in opioid crisis. Effects of fentanyl overdose-induced muscle rigidity and medetomidine on respiratory mechanics and pulmonary gas exchange in sedated rats. Respiratory effects of thyrotropin-releasing hormone and its analogue taltirelin on opioid-induced respiratory depression. Difficult or impossible ventilation after sufentanil-induced anesthesia is caused primarily by vocal cord closure. Fentanyl causes naloxone-resistant vocal cord closure: A platform for testing opioid overdose treatments. Adapt Pharma Inc. Accessed December 24, US Food and Drug Administration. Accessed January 5, FDA approves higher dosage of naloxone nasal spray to treat opioid overdose. Opioid antagonists from the orvinol series as potential reversal agents for opioid overdose. Methocinnamox reverses and prevents fentanyl-induced ventilatory depression in rats. Covalently loaded naloxone nanoparticles as a long-acting medical countermeasure to opioid poisoning. All Rights Reserved. View Metrics. Citing articles via Web Of Science Uptake of Halothane by the Human Body. Email alerts Article Activity Alert. Online First Alert. Anesthesiology Featured Articles Alert. Social Media Twitter. Anesthesiology ASA Monitor. Cookie Settings. Close Modal.

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