[The role of cholinergic regulation of the heart in the protective antiarrhythmic effect of adaptation to continuous moderate stress].
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Biomedical subjects
Publications and source records attributed to K B Vinnitskaia.
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The effect of left-ventricular myocardial infarction (MI) on cholino- and adrenoreactivity of an isolated right atrium and acetylcholine (AC) content of both atria was evaluated experimentally in Wistar rats, adapted or unadapted (control) to stress. In the control sample, 24-hour-long MI increased the chronotropic response to AC, while atrial endogenic AC dropped fourfold. Those changes were accompanied by no marked changes in pacemaker adrenoreactivity. Adaptation to stress reduced pacemaker choline reactivity without any significant effect on pacemaker adrenoreactivity or atrial AC. At the same time, adaptation largely prevented MI-induced increase in pacemaker choline reactivity and atrial AC drop. Increased pacemaker choline reactivity, seen in MI, enhances pacemaker sensitivity to cognition of ectopic excitation foci and, hence, cholinergic effects, that may promote the emergence of arrhythmia. Therefore, pacemaker resistance to cholinergic action, increasing in the course of adaptation, may be an important element of the protective antiarrhythmic effect of adaptation to stress in MI.
The effect of left ventricular experimental infarction (caused by left coronary artery ligation) on the isolated right atrium contractile function and acetylcholine content in both atria was studied in male Wistar rats. It was shown that a 24-hour infarction induced an increase in atrial chronotropic response to acetylcholine, which proved an increase in the pacemaker cholinoreactivity. Atrial inotropic response to acetylcholine characterizing the contractile myocardium cholinoreactivity remained unchanged. At the same time atrial endogenous acetylcholine content decreased fourfold. An increase in pacemaker cholinoreactivity was not accompanied by changes in its adrenoreactivity; those changes increased the pacemaker sensitivity to cholinergic influences which could help elucidate the ectopic excitation foci, thus promoting the onset of arrhythmia.
Four-percent carbon dioxide added to the gaseous medium during swimming exercise under normoxia increased animals' working capacity, myocardial contractility, the stability of myocardial acetylcholine store and cardiac choline reactivity, and contributed to post-exercise retention of those changes. Three months' training under the same conditions caused no further increment in adaptation parameters, while potentialities of the parasympathetic regulation mechanism even declined, and the acquired changes were promptly lost upon discontinuation of exercise. Mechanisms of action and significance of carbon dioxide in the formation of adaptation and after-effect circulatory stability are discussed.
4% CO2 addition to normoxic gas medium increased the activity, mass and functional capacity of the left ventricular myocardium, enhanced the stability of acetylcholine (AC) and noradrenaline (NA) storage in the myocardial tissues and stimulated myocardial response to these mediators during physical training of rats (swimming for 2 months). When the duration of the training period was prolonged to 3 months, CO2 had a decreasing effect on the myocardial activity, AC concentration and storage stability, as well as on the myocardial response to AC. The possibility of reducing signal and increasing metabolic CO2 effects during physical training is considered. The importance of intensified heart regulation by sympathetic and parasympathetic mechanisms during adaptation and the role of mechanism dissociation with the decrease in the degree of adaptation are discussed.
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A procedure is described for the radioisotope assay of acetylcholine transferase activity (EC 2.3.1.6), which involved specific synthesis of acetylcholine in vivo. Bromine acetylcholine was used as an inhibitor of the enzyme; 14C-AcCoA was used as a substrate and product of the enzymatic reaction. 14C-acetylcholine was separated from the substrate by means of anion exchange chromatography. The procedure described was 5 times more sensitive than the methods developed by F. Fonnum (1975) and S. Tucek (1983) being similarly reproducible. The assay was tested in experiments with rats under various conditions of hyperbaric oxygenation, in simulation of myocardial infarction as well as in moderate immobilization stress. The findings suggest that estimation of the acetylcholine transferase activity may be involved in complex evaluation of the cholinergic system state in tissues, which is essential for the study of pathogenesis of their dysfunctions and development of respective approaches to eliminate these impairments.