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Opiate Antagonist (opiate + antagonist)
Selected AbstractsUltra-rapid opiate detoxification: from clinical applications to basic scienceADDICTION BIOLOGY, Issue 2 2003EMMANUEL STREEL Rapid or ultra-rapid opiate detoxification has become increasingly popular in both private and public addiction centres. These techniques seem to facilitate the transfer of opiate-dependent patients from opiate agonist to opiate antagonist. Despite the probable complex neuropharmacological aspects involved in these procedures, their development over nearly three decades is notable for the almost complete absence of clinically relevant animal studies. This paper discusses the historical background of this occurrence, and reviews the small number of animal studies that have been conducted. Many discussions and arguments about the techniques seem to underscore their true purpose, which is not "simply to detoxify" opiate-addicted patients but to initiate long-term management with naltrexone. For this reason, it may be better to conceptualize these techniques not as "rapid detoxification" but as "rapid antagonist induction". [source] Preclinical and clinical pharmacology of alcohol dependenceFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 1 2007Sophie Tambour Abstract In recent years, advances in neuroscience led to the development of new medications to treat alcohol dependence and especially to prevent alcohol relapse after detoxification. Whereas the earliest medications against alcohol dependence were fortuitously discovered, recently developed drugs are increasingly based on alcohol's neurobiological mechanisms of action. This review discusses the most recent developments in alcohol pharmacotherapy and emphasizes the neurobiological basis of anti-alcohol medications. There are currently three approved drugs for the treatment of alcohol dependence with quite different mechanisms of action. Disulfiram is an inhibitor of the enzyme aldehyde dehydrogenase and acts as an alcohol-deterrent drug. Naltrexone, an opiate antagonist, reduces alcohol craving and relapse in heavy drinking, probably via a modulation of the mesolimbic dopamine activity. Finally, acamprosate helps maintaining alcohol abstinence, probably through a normalization of the chronic alcohol-induced hyperglutamatergic state. In addition to these approved medications, many other drugs have been suggested for preventing alcohol consumption on the basis of preclinical studies. Some of these drugs remain promising, whereas others have produced disappointing results in preliminary clinical studies. These new drugs in the field of alcohol pharmacotherapy are also discussed, together with their mechanisms of action. [source] Neural Circuits Regulating Pulsatile Luteinizing Hormone Release in the Female Guinea-Pig: Opioid, Adrenergic and Serotonergic InteractionsJOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2001A. C. Gore Abstract We studied three neurotransmitters involved in the regulation of pulsatile luteinizing hormone (LH) release: opioid peptides, serotonin and norepinephrine, using the ovariectomized guinea-pig. This is an attractive animal model due to the regularity of its LH pulses, enabling any disruptions to be clearly ascertained. In all experiments, a specific agonist or antagonist was administered, either alone or serially to enable detection of interactions, and effects on mean LH concentrations, pulse amplitude and interpulse interval were determined by PULSAR analysis. In the ovariectomized guinea-pig, catecholamines are stimulatory (acting through the ,1 and ,2 but not , receptors, unlike other species), opioids inhibitory and serotonin permissively stimulatory to pulsatile LH release. Stimulatory effects of the opiate antagonist were not blocked by pretreatment with an ,1 - or ,2 -adrenergic antagonist. Similarly, pretreatment with the opiate antagonist did not prevent the suppression of LH release by ,1 and ,2 antagonists. This suggests that, in the guinea-pig, effects of opiates and catecholamines on LH release are exerted by independent pathways to luteinizing hormone releasing hormone (LHRH) neurones. For the opiate,serotonin interactions, pretreatment with the serotonergic antagonist did not block the stimulatory effect of the opiate antagonist on LH release. However, pretreatment with the opiate agonist could not be overcome by the serotonergic agonist. This suggests that the effects of the serotonin system on LHRH release may be indirectly mediated by opioid neurones. Taken together, these studies demonstrate that the three neurotransmitter systems studied are critically involved in normal pulsatile LH release in the female guinea-pig, and demonstrate novel functional relationships between the opioid and the adrenergic and serotonergic systems. [source] Safe reduction in administration of naloxone to newborn infants: An observational studyACTA PAEDIATRICA, Issue 9 2006Deborah Box Abstract Background: Naloxone, a specific opiate antagonist, is widely used during neonatal resuscitation to reverse possible opiate-induced respiratory depression. Aim: To determine the frequency with which naloxone is administered when resuscitation guidelines are conscientiously followed and to document any effect on respiratory morbidity. Methods: Perinatal data including naloxone administration and respiratory morbidity were collected retrospectively, and compared with prospectively collected data following the introduction of "Good Practice" guidelines. Results: There were 500 deliveries in the retrospective arm of the study and 1000 deliveries in the prospective arm. Although a similar proportion of women received opiates in labour in the two periods of study, there was a marked reduction in the use of naloxone when the guidelines were introduced (11% of opiate-exposed deliveries compared to 0.2%). There was no significant effect on respiratory morbidity with the change in practice. Conclusion: Naloxone is rarely needed to reverse the effects of opiates in newborn infants, and its use can be curtailed by following current resuscitation guidelines without increasing respiratory morbidity. [source] Effect of Naloxone on Appetitive and Consummatory Phases of Ethanol Self-AdministrationALCOHOLISM, Issue 7 2001Amanda L. Sharpe Background : The opioid system has been implicated in ethanol self-administration. Morphine, an opiate agonist, can sometimes increase the amount of ethanol consumed, and opiate antagonists such as naloxone and naltrexone decrease the amount of ethanol consumed in both animals and humans. The objective of this study was to examine the effect of naloxone on appetitive (or seeking) and consummatory behaviors by using an operant model developed to separate these two phases of self-administration. Methods: Intraperitoneal injections of naloxone (0.3,10 mg/kg) or vehicle were given before operant self-administration sessions to assess the effect on lever pressing (appetitive behavior) and subsequent consumption. Effects were measured in two groups of rats: one self-administered a 3% sucrose solution and the other a 10% ethanol solution. Results: Naloxone dose-dependently decreased ethanol and sucrose consumption by an earlier cessation of drinking in the session compared with vehicle injection days. There were some effects on appetitive responding after treatment with naloxone, but none was statistically significant. Conclusions: Naloxone may decrease ethanol self-administration by decreasing the postingestive or pharmacological effects of alcohol. This model provides a new method for examining the effects of potential pharmacotherapeutics on alcohol self-administration behavior. [source] New Developments in the Pharmacotherapy of Alcohol DependenceTHE AMERICAN JOURNAL ON ADDICTIONS, Issue 2001Hugh Myrick M.D. Neuroscientific underpinnings and pharmacotherapeutic treatments of sub-stance use disorders are rapidly developing areas of study. In particular, there have been exciting new developments in our understanding of the involvement of excitatory amino acid neurotransmitter systems and the opiate and serotonin systems in the pathophysiology of alcohol withdrawal, alcohol dependence, and in subtypes of individuals with alcoholism. In this article, new developments in the pharmacotherapy of alcohol dependence will be reviewed. In particular, the use of anticonvulsants in alcohol withdrawal and protracted abstinence syndromes will be discussed. New data on opiate antagonists and acamprosate, an agent that exerts actions through excitatory amino acid systems in relapse prevention, will be reviewed. Finally, there will be a review of new data concerning the use of serotonin reuptake inhibitors in subtypes of alcoholism and the use of combination pharmacotherapy. [source] Lofexidine for opiate detoxificationACTA NEUROPSYCHIATRICA, Issue 5 2004Jenny Bearn The evolving role for lofexidine in the treatment of opiate detoxification over the last decade is reviewed. Lofexidine is no better than methadone or clonidine in attenuating withdrawal symptom severity, although it has a more favourable side-effect profile than clonidine. In conjunction with opiate antagonists, lofexidine may facilitate accelerated withdrawal, although activity and low liability for misuse, lofexidine may be more widely acceptable to clinicians than methadone, particularly those working in out-patient, non-specialist and prison treatment settings. Further studies in these treatment settings will be particularly apposite since, apart from the studies highlighted, the evidence base for the clinical value of lofexidine is mainly to be derived from in-patient trials. [source] | ||||||||||