Introduction: Opioid dependence is recorded as the most common drug of abuse in Malaysia. Currently, the preferred substitution therapy for most Government treatment centres is methadone used as substitution therapy for opioid dependence. There are, however patients who may benefit from being on the combined buprenorphine-naloxone formulation as substitution therapy instead. We discuss six cases of opioid dependence of varied backgrounds that were treated with buprenorphinenaloxone therapy and their outcomes. Discussion: All of the reported patients improved after the induction of buprenorphine- naloxone. Two of the cases highlighted the transfer of patients on methadone to buprenorphine-naloxone due to the adverse effect and interactions of methadone with other medications. During the transfer there were no major adverse reactions noted, and patients were safely able to continue with the maintenance therapy of buprenorphine- naloxone. Conclusion: Buprenorphine-naloxone is a safe and effective drug substitution therapy for opioid dependence. It has fewer interactions with other medications, and has similar efficacy to methadone. Being a partial agonist, it has a less sedating effect making patients more functional.
Buprenorphine, Naloxone Drug Combination

62 patients with opiod poisoning involved our study were treated by naloxon and respiratory supportive therapies as united protocol. Because of aggressive using naloxon, the ratio of patients requiring intubations and mechanical ventilation was significantly decreased, 29% and 17.7% respectively. The manifestation of opiod overdose were rapidly improved and almost of the patients (95.5%) were treated successfully. The side effects of naxolon were minor. We observed only 2 cases having vomiting after Iv injection of naloxon. Ambuballon bagging with 100% oxygen was mainly respiratory supportive therapy. The mechanical ventilation indicated for the patients suffering from life-threatening respiratory failure. Heroin-induced pulmonary edema accounted for 82% of these cases. PEEP was used in 7 patients. The mean of PEEP levels was 5.31.3 cmH2O. Our protocol was success in 95.5%.
Poisoning ; Naloxone ; therapeutics

Opioids are the one of the most commonly used drugs to control cancer pain all over the world. But, we should not overlook the potential risk of opioid intoxication because they have well-known detrimental side effects. The opioid intoxication can be diagnosed thorough various clinical manifestations. The altered mental status, respiratory depression, and miosis is very representative clinical features although these symptoms don't always appear together. Unfortunately the opioid-toxidrome can be varied. A 42 years old man came to our emergency room after taking about 900 mg morphine sulfate per oral. He was nearly alert and his respiration was normal. Even though his symptoms didn't deteriorated clinically, serial arterial blood gas analysis showed increase in PaCO2. So we decided to use intravenous naloxone. Soon, he was fully awaked and his pupils size was increased. After a continuous infusion of intravenous naloxone for 2 hours, PaCO2 decreased to normal range and his pupil size also returned to normal after 12 hours. Though the levels of serum amylase and lipase increased slightly, his pancreas was normal according to the abdominal computed tomography. He had nausea, vomit, and whole body itching after naloxone continuous infusion, but conservatively treated. We stopped the continuos infusion after 1 day because his laboratory results and physical examinations showed normal. As this case shows, it is very important to prescribe naloxone initially. If you suspect opioid intoxication, we recommend the initial use of naloxone even though a patient has atypical clinical features. In addition, we suggest intranasal administration of naloxone as safe and effective alternative and it's necessary to consider nalmefene that has a longer duration for opioid intoxication.
Administration, Intranasal ; Amylases ; Analgesics, Opioid ; Blood Gas Analysis ; Emergencies ; Humans ; Lipase ; Miosis ; Morphine ; Naloxone ; Naltrexone ; Nausea ; Pancreas ; Physical Examination ; Porphyrins ; Pruritus ; Pupil ; Reference Values ; Respiration ; Respiratory Insufficiency

We provide the reader with a brief introduction to the neurobiology of neuropeptides. Several comprehensive reviews of the distribution and neurochemical. neurophysiological. neuropharmacological and behavioral effects of the major neuropeptides have recently appeared. In reviews of the large number of neuropeptides in brain and their occurance in brain regions thought to be involved in the pathogenesis of major psychiatric disorders, investigators have sought to determine whether alternations in neuropeptide systems are associated with schizophrenia, mood disorders, anxiety disorders, alcoholism and neurodegenerative disease. There is no longer any doubt that neuropeptide-containing are altered in several neuropsychiatric disorders. One of the factors that has hindered neuropeptide research to a considerable extent is the lack of pharmacological agents that specifically alter the synaptic availability of neuropeptides. With the exception of naloxone and naltrexone, the opiate-receptor antagonists, there are few available neuropeptide-receptor antagonists. Two independent classes of neuropeptide-receptor antagonists has been expected to be clinically useful. Naltrexone a potent micro-receptor antagonist has been used successfully to reduce the need for alcohol consumption. And cholecycstokinin antagonists are now in development as a new class of anxiolytics, which would be expected to be free from tolerance and physical dependence and lack of sedation. In this review, we deal with these two kinds of neuropeptide system, the opioid system and cholesystokinins in the brain. The role of opioid systems in the reinforcement after alcohol consumtion and that of cholesystokinins in the pathogenesis of anxiety will be discussed briefly. As we know, the future for neuropeptides in psychiatry remains bright indeed.
Alcohol Drinking ; Alcoholism ; Anti-Anxiety Agents ; Anxiety ; Anxiety Disorders ; Brain ; Cholecystokinin* ; Endorphins* ; Humans ; Mood Disorders ; Naloxone ; Naltrexone ; Neurobiology ; Neurodegenerative Diseases ; Neuropeptides* ; Panic ; Research Personnel ; Schizophrenia

No abstract available.
Colon* ; Humans* ; Morphine* ; Naloxone* ; Perfusion*

No abstract available.
Animals ; Meperidine* ; Mice* ; Morphine* ; Naloxone*

BACKGROUND: WIN55212-2 is a synthetic cannabinoid agonist and selective to cannabinoid 1 (CB1) receptors, which are distributed mainly in the central nervous system. Opioid receptors and CB1 receptors have several similarities in terms of their intracellular signal transduction mechanisms, distributions, and pharmacological action. Several studies have therefore sought to describe the functional interactions between opioids and cannabinoids at the cellular and behavioral levels. The present study investigated agonist-stimulated [35S]GTPgammaS binding by WIN55212-2 in rat brain membranes and determined the antagonism by selective opioid antagonists at the level of receptor-ligand interaction and intracellular signal transduction. METHODS: Sprague-Dawley rats (male, n = 20) were euthanized for the preparation of brain membranes. In agonist-stimulated [35S]GTPgammaS binding by WIN55212-2, the values of EC50 and maximum stimulation (% over basal) were determined in the absence or presence of the micro, kappa and delta opioid receptor antagonists naloxone (20 nM), norbinaltorphimine (3 nM), and naltrindole (3 nM), respectively. Ke values for opioid antagonist inhibition in the absence or presence of each opioid receptor antagonist were calculated using the following equation: [nanomolar antagonist] / (dose ratio of EC50 - 1). RESULTS: In WIN55212-2-stimulated [35S]GTPgammaS binding in the rat brain membranes, the values of EC50 and maximum stimulation (% over basal) were 154 +/- 39.5 nM and 27.6 +/- 5.3% over basal, respectively. Addition of selective opioid antagonists did not produce a significant rightward shift in the WIN55212-2 concentration-response curve, and Ke values were not applicable. CONCLUSIONS: Our results suggest that the functional activity of WIN55212-2-stimulated [35S]GTPgammaS binding was not affected by opioid antagonists in the rat brain membranes. Although the exact mechanism remains unclear, our results may partially elucidate their actions.
Analgesics, Opioid ; Animals ; Benzoxazines ; Brain ; Cannabinoids ; Central Nervous System ; Membranes ; Morpholines ; Naloxone ; Naltrexone ; Naphthalenes ; Narcotic Antagonists ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1 ; Receptors, Opioid ; Receptors, Opioid, delta ; Signal Transduction

BACKGROUND: It is generally accepted that morphine affords cardioprotection against ischemia/reperfusion injury. Inhibition of the mitochondrial permeability transition pore (MPTP) is considered an end target for cardioprotection. The aim of this study was to investigate the involvement of opioid receptors (OR) and MPTP in morphine-induced postconditioning (M-Post). METHODS: Isolated rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Hearts were treated with 1 microM morphine, with or without the OR antagonists or a MPTP opener at early reperfusion. Infarct size was measured with 2,3,5-triphenyltetrazolium chloride staining. RESULTS: There were no significant differences in cardiodynamic variables except a decrease in heart rate in the M-Post group (P < 0.01 vs. control) after reperfusion. M-Post dramatically reduced infarct-risk volume ratio (9.8 +/- 2.5%, P < 0.001 vs. 30.0 +/- 3.7% in control). This beneficial effect on infarct volume by M-Post was comparable with ischemic postconditioning (11.9 +/- 2.2%, P > 0.05). The nonspecific OR antagonist naloxone (25.7 +/- 1.9%, P < 0.01), the delta-OR antagonist naltrindole (27.8 +/- 4.3%, P < 0.05) and delta1-OR antagonist 7-benzylidenenaltrexone (24.7 +/- 3.7%, P < 0.01) totally abrogated the anti-infarct effect of M-Post. In addition, the anti-infarct effect by M-Post was also totally blocked by the MPTP opener atractyloside (26.3 +/- 5.2%, P < 0.05). CONCLUSIONS: M-Post effectively reduces myocardial infarction. The anti-infarct effect by M-Post is mediated via activation of delta-OR, especially delta1-OR, and inhibition of the MPTP opening.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Animals ; Atractyloside ; Benzylidene Compounds ; Heart ; Heart Rate ; Ischemia ; Ischemic Postconditioning ; Mitochondrial Membrane Transport Proteins ; Morphine ; Myocardial Infarction ; Naloxone ; Naltrexone ; Permeability ; Rats ; Receptors, Opioid ; Reperfusion ; Reperfusion Injury ; Tetrazolium Salts

No abstract available.
Adolescent* ; Humans ; Naloxone* ; Self-Injurious Behavior*

No abstract available.
Analgesia* ; Animals ; Fenclonine* ; Mice* ; Naloxone* ; Swimming*