beta-endorphin and Arrhythmias--Cardiac

There is substantial evidence that cardiac opioid receptors are activated during arrhythmias induced by administration of opioid peptides or myocardial ischemia, supporting the hypothesis that endogenous opioid peptides (EOP) are involved in myocardial infarction. This prospective clinical trial is designed to determine whether the ischemia-induced arrhythmias and extent of the infarct are related to the release of the EOP beta-endorphin in patients with acute myocardial infarction. Two groups were included in the study, patients with acute myocardial infarction, and healthy volunteers who served as controls. The results indicate that, compared to the controls, there was augmentation of ischemic arrhythmias and ischemic damage as assessed by serum creatine kinase activity, accompanied by an elevated level of beta-endorphin, in patients with acute myocardial infarction. The above data strongly indicate that EOP are indeed involved in the pathophysiology of myocardial infarction, and suggest these peptides have an important role in ischemic heart disease.

Topics: Aged; Arrhythmias, Cardiac; beta-Endorphin; Creatine Kinase; Electrocardiography; Female; Humans; Isoenzymes; Male; Myocardial Infarction; Prospective Studies

The objective of this study was to examine the involvement of endogenous opioid peptides and opioid receptor (OR) subtypes in the cardioprotective effect of adaptation to chronic hypoxia in rats.. Rats were exposed to continuous normobaric hypoxia (CNH; 12% oxygen) for 3 weeks. Myocardial ischemia was induced by 20-min coronary artery occlusion followed by 3-h reperfusion in anesthetized open-chest animals. Various OR antagonists were administered to rats prior to ischemia. The size of myocardial infarction and the incidence of ischemic ventricular arrhythmias were assessed. Myocardial and plasma concentrations of opioid peptides (met-enkephalin, β-endorphin, and endomorphins) were determined.. Adaptation to CNH significantly increased myocardial and plasma concentrations of opioids, potentiated their further elevation by ischemia/reperfusion, and reduced myocardial infarct size, but it did not affect the incidence of ischemic arrhythmias. The infarct size-limiting effect of CNH was abolished by OR antagonists naltrexone (non-selective), naloxone methiodide (non-selective peripherally acting), TIPP[ψ] (δ-OR), naltriben (δ2-OR), or CTAP (μ-OR), while BNTX (δ1-OR) and nor-binaltorphimine (κ-OR) had no effect.. The results suggest that the infarct size-limiting effect afforded by adaptation to CNH is mediated by activation of peripheral δ2- and μ-ORs by elevated levels of endogenous opioid peptides.

Topics: Adaptation, Physiological; Animals; Arrhythmias, Cardiac; beta-Endorphin; Enkephalin, Methionine; Hypoxia; Male; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion Injury; Narcotic Antagonists; Oligopeptides; Rats; Rats, Wistar; Receptors, Opioid, delta; Receptors, Opioid, mu

Topics: Animals; Arrhythmias, Cardiac; Autonomic Nervous System; beta-Endorphin; Cats; Female; Heart; Male; Myocardial Ischemia

Adaptation to intermittent hypoxia had a pronounced antiarrhythmic effect in acute myocardial ischemia in conscious animals. This effect was less pronounced in anesthesia and was absent in isolated heart. In reperfusion, the prophylactic effect of adaptation was equally pronounced in all cases. Adaptation prevented stress-induced exhaustion of brain beta-endorphine presumably by its accumulation in adrenal glands and resulted in the accumulation of dopamine, 5-hydroxytryptamine and 5-hydroxyindolacetic acid in brain structures. These data naturally lead to the assumption that central mechanisms play the main role in the antiarrhythmic effect of adaptation to intermittent hypoxia on ischemic arrhythmias, while mechanisms occurring at the level of heart play the main role in the protective effect of the same adaptation against reperfusion arrhythmias.

Topics: Acclimatization; Adrenal Glands; Altitude; Animals; Arrhythmias, Cardiac; beta-Endorphin; Brain; Coronary Disease; Hypoxia; Male; Myocardial Reperfusion; Neurotransmitter Agents; Organ Specificity; Rats; Rats, Inbred Strains; Reference Values

It was shown that adaptation to intermittent hypoxia in altitude chamber prevented the poststress fall of the electrical threshold of heart fibrillation. In acute ischemia, the number of fibrillation episodes and the death rate of preadapted animals were 2-3 fold lower than in controls. The adaptation to hypoxia resulted in a significant increase in concentration of opioid peptide beta-endorphin in adrenal glands while stress-induced changes in beta-endorphin in brain structures of adapted animals were much less pronounced. In animals with postinfarction cardiosclerosis, the course of hypoxic actions resulted in restoration of the decreased heart fibrillation threshold, reduced the heart ectopic activity which had developed on the background of vagal bradycardia, and eliminated depression of the heart contractile function. Simultaneously, the adaptation induced a decrease of the postinfarction scar by one-third and an increase of vascularization of the myocardial zone adjacent to the scar.

Topics: Adaptation, Physiological; Altitude; Animals; Arrhythmias, Cardiac; beta-Endorphin; Brain Chemistry; Coronary Disease; Myocardial Infarction; Oxygen; Rats; Rats, Inbred Strains; Stress, Physiological

The intravenous administration of naloxone 15 min before acute coronary artery ligation in both anesthetized and conscious male rats markedly reduced the incidence and severity of the ventricular arrhythmias that occur within 30 min of the onset of myocardial ischaemia. The incidence of ventricular fibrillation was especially reduced and, in conscious rats, the survival 16 h after ligation was increased from 27% (in the controls) to 58 and 73% after 2 and 4 mg/kg naloxone respectively. One possible explanation of these results implies a detrimental effect of released endorphin in the early stages of myocardial ischaemia.

Topics: Anesthesia; Animals; Arrhythmias, Cardiac; beta-Endorphin; Coronary Vessels; Endorphins; Ligation; Male; Naloxone; Rats; Rats, Inbred Strains; Time Factors