Biomedical subjects
Publications and source records attributed to L N Maslov.
Blockade of the mu and delta receptors exerted no effect upon the heart resistance against arrhythmogenic influences. Stimulation of the delta receptors increased the myocardial resistance against arrhythmogenic influences. Autonomic nervous system seems to take no part in this effect.
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1. The influence of acute myocardial ischaemia (AMI) complicated by ventricular fibrillation (VF) on opioid peptide level in myocardium and blood plasma of rats has been studied. 2. Leu-enkephalin level in myocardium of rats with AMI and VF has been found to be significantly lower than in animals with AMI but without VF. 3. Met-enkephalin level has been found to be significantly increased in both animals with VF and without it. We have not found a significant difference in met-enkephalin level in myocardium of animals with VF and without it. 4. AMI was induced to increase the enkephalin and beta-endorphin level in blood plasma of all the animals, whether VF had occurred or not. 5. Preliminary administration of D-Ala2,Leu5,Arg6-enkephalin, a synthetic analogue of leu-enkephalin, has prevented a decrease of ventricular fibrillation threshold in experimental coronary occlusion. 6. The obtained results allow us to conclude that enkephalins of myocardium but not opioid peptides of blood plasma play an important role in VF occurrence.
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We studied antiarrhythmic action of D-Ala 2, Leu 5, Arg 6-enkephalin (dalargin) in experiments on male rats. Dalargin is reported to prevent heart rhythm disturbance and heart electrical stability decrease in experimental coronary occlusion, postinfarction, cardiosclerosis and emotional stress. Dalargin prevents acute myocardial ischaemia-induced increase of cAMP content in blood serum and cardiac muscle, as an indirect feature of its antiadrenergic activity. D-Ala 2, Leu 5, Arg 6-enkephalin leads to a decrease of cAMP content in myocardium and blood plasma, which presumably indicates a decrease of sympathetic tone. The data strongly suggest that cGMP content increase and somatostatin level decrease in cardiac muscle play a significant role in antiarrhythmic action of dalargin.
Enkephalins were injected intravenously at a dose of 0.1 mg/kg 15 minutes or 6 hours before adrenalin or CaCl2 injection. Enkephalins were reported to prevent adrenal ventricular extrasystoles but not to influence CaCl2-induced dysrhythmias. Maximum antiarrhythmic effect of enkephalins was demonstrated 6 hours later after the intravenous injection. Naloxone at a dose of 2 mg/kg and morphine at a dose of 1.5 mg/kg prevent adrenal arrhythmias 15 min and 6 hours later after injection. We believe that peripheral delta opiate receptors activation by enkephalins as well as the blockade of non-identified opiate receptors by naloxone prevent arrhythmias.
A course injection of Rhodiola rosea extract for eight days was reported to increase the resistance of experimental animals to adrenalin- or CaCl2-induced arrhythmias. Preliminary injection of naloxone in a dose of 0.5 mg/kg eliminated the antiarrhythmic effect of Rhodiola. Indomethacin had no effect the antiarrhythmic action of Rhodiola. The antiarrhythmic effect of Rhodiola course injections was assumed to be associated with the induction of opioid peptides biosynthesis.
The experiments performed on emotional--painful stress model in rats demonstrated cardioprotective activity of adaptogens of vegetable origin (rodiolae, eleutherococcus, levsea, p-tyrosol). Preliminary injection of rodiolae extract was found to prevent stress--induced increase in cAMP level and cGMP content decrease in heart. We can conclude that adaptogens cardioprotective effect may be the drugs to prevent stressor change in cyclic nucleotides level in myocardium.
It has been established that preliminary administration of D-Ala2-Leu5-Arg6-enkephalin, D-Met2-Pro5-enkephalinamide, and D-phenylalanine to experimental animals prevents a stress-induced increase of the content of thromboxane in the blood plasma and myocardium and induces a rise of the level of prostacyclin, PGF2 and PGE in the heart and blood plasma. The authors hold that the changes in the level of prostanoids may mediate cardioprotective and anti-stressor rather than antiarrhythmic effects of enkephalins.
Adaptation of rats to cold and physical exercise prevented ventricular fibrillation (VF) caused by the occlusion of the left anterior coronary artery. In the heart of adapted rats with acute myocardial ischemia, myocardial enkephalins increased whereas the level of cAMP declined as compared to nonadapted animals. Injection of dalargin before the occlusion of the coronary artery in rats prevented both VF and a decrease of VF threshold. The peptide averted the rise of cAMP content in the heart during acute myocardial ischemia. The data obtained suggest that the rise of endogenous myocardial enkephalins may have an important role in antiarrhythmic action of adaptation. It is assumed that antiarrhythmic effect of enkephalins may be related to the restriction of sympathetic influence on the heart.
It was found, that injection of delta-receptors agonist dalargin before the occlusion of left anterior coronary artery in rats prevented the decrease of ventricular fibrillation threshold (VFT). An injection of naloxone in dose 0.5 mg/kg (for the blockade of mu-receptors only) had no influence on the VFT. Naloxone in dose 1 mg/kg (for the blockade peripheric mu- and delta-receptors) decreased VFT. An intraventricular infusion of dalargin (10 mkg) induced bradycardia and an increase of VFT. It was assumed that anti-arrhythmic effects of enkephalins in acute myocardial ischemia could be realized by an activation of peripheric delta-receptors and central mu-receptors.
It was found, that adaptation of rats to cold and physical exercise prevented ventricular fibrillation, caused by the occlusion of the left anterior coronary artery. An adaptation to cold only or to physical exercise do not prevent ventricular arrhythmias. An significant increase of prostacyclin/thromboxane index in plasma and heats was estimated in rats adapted to cold and physical exercise in relation to control non-adapted group in condition of functional rest or acute myocardial ischemia. It was assumed that an increase of prostacyclin/thromboxane ratio has a significant role in antiarrhythmic action of adaptation.
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Ventricular fibrillation, caused by the occlusion of the anterior descending coronary artery, results in leu-enkephalin level decrease in ischemic and non-ischemic zones of myocardium. The fibrillation is found to induce cAMP increase in the ischemic zone and cGMP increase in the normal circulation zone. cGMP and leu-enkephalin level correlates with fibrillation duration. Enkephalins and cyclic nucleotides are suggestive of being of importance in heart rythm disturbances pathogenesis.