Effect of preliminary adaptation to moderate and intensive physical loads on cardiac electrical stability and contractile function in experimental myocardial infarct

Preliminary adaptation of animals to a moderate swimming exercise prevented the fall of ventricular fibrillation electrical threshold and limited drastically the heart ectopic activity in acute myocardial infarction. Adaptation to intense stress, i.e. prolonged swimming with a load, had less preventive effect. The rationing of preventive exercise, to be used for the prophylaxis of myocardial infarction, is discussed.     

Prevention of heart damage by extreme physical stress and increasing its resistance to acute overstrain with the antioxidant ionol

A study of the effect of extreme physical stress on the contractility of an isolated heart, its CPK loss associated with anoxia and reoxygenation, and myocardial adenyl components and lactate levels under acute overstrain of the heart achieved through a complete obstruction of the aorta, showed the animals doing exercise to have reduced cardiac contractility, increased perfusate CPK waste, and sharply decreased myocardial macroergic phosphate levels under acute overstrain by pressure. Pretreatment with ionol largely prevented these changes.     

Comparative evaluation of the effect of preliminary adaptation of the body to moderate physical loading and brief stress exposures on heart contractile function disorders in long-term stress

The effect of repeated emotional-painful stress stimuli and repeated moderate exercise (swimming) on cardiac resistance to long-term emotional-painful stress (EPS) was studied in Wistar rats. Adaptation to repeated exercises was found to significantly increase tension developed by the myocardium of an isolated auricle and myocardial resistance to hypoxia and excessive calcium, but it could not prevent the EPS-induced depression of contractility. Adaptation to short-term stress on the contrary, did not significantly affect myocardial tension and cardiac resistance to hypoxia and excessive calcium, but it completely prevented the long-term EPS-induced depression and considerably reduced the stress-potentiating effect on the development of calcium and hypoxic contractures. Therefore, adaptation to stressful effects proper, rather than moderate exercise, can build up heart resistance to damaging stress effects.     

Prevention of stress-induced and hypoxic heart lesions by means of an antioxidant ionol

It was shown in experiments on male Wistar rats that activation of peroxidized oxidation of myocardial lipids and accumulation of hydroperoxides in the myocardium comprise the decisive link of the pathogenic chain of stress and hypoxic damages to the heart. Injection of a potent non-toxic antioxidant into the animals before exposure to the stress or hypoxia blocks the activation of peroxidized oxidation and prevents disorder of the contractile function and damage to the heart muscle appraised according to the elimination of enzymes from the myocardial cells.     

Prevention of disorders of myocardial contractile function under stress by the preliminary adaptation of animals to physical load

Rats adapted to exercise (daily swimming for one hour over 30 days) and control animals were subjected to emotional-painful stress (EPS) according to the pattern of anxiety neurosis. It has been established that EPS decreases the amplitude as well as the rate of contractions and relaxations of the isolated papillary muscles of animals by 2-3 times and also reduces the resistance of the contractile function of the myocardium to the excess of Na+ and H+ ions, ousting Ca2+ from the sites of its binding in the sarcolemma. Adaptation to exercise exerts an opposite effect. The preliminary adaptation of animals prior to EPS prevents or limits the stress-related depression of the contractility of the myocardium and the diminution of its resistance to the factors replacing Ca2+. The preliminary adaptation to exercise may be used for preventing stress-related disorders of cardiac contractility.     

Effect of adaptation to stress exposures on the cholino- and adrenoreactivity of the atria and their content of acetylcholine in rats with myocardial infarct

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.     

Prevention of cardiac fibrillation using antioxidants and preliminary adaptation of animals to the effects of stress

Electrical ventricular fibrillation threshold (VFT) was determined, using programmed isolated stimuli on the left-ventricular apex, in male Wistar rats at different times after 10 hours' immobilization stress (IS). The VFT decrease reached a maximum of 48% 12 hours after IS. Cardiac sensitivity to the inhibiting vagal influence was increased considerably at the same time. The adaptation to short episodes of IS over 6 days, intermittent exposure to high-altitude hypoxia (5 hours daily at a 5000 m "altitude" for 40 days) and the antioxidant ionol (50 mg/kg) prevented IS-induced fibrillation threshold decrease. In cases of coronary arterial ligation in waking animals, the antioxidant ionol reduced fourfold the mortality associated with ventricular fibrillation and raised the spontaneous defibrillation rate from 28% to 72%. Possible mechanisms of these phenomena are discussed.     

Automated mapping of the heart electrical potentials in myocardial infarct patients

A method is developed for automated cartography of the heart's electric potentials from 90 points on the chest surface. The input data program determines characteristic QRS profiles on the basis of change in the value of the first derivative, labelling the identifiable characteristic outlines, computes the gradients for Q/R, R/S amplitude ratios for every element of the field and estimates zone area for each gradient and mean Q, R, S wave amplitudes for all points within the field.     

Evaluation of the reserve capacity of the heart in acute myocardial infarct by creating a brief volume load

A combination of non-invasive and invasive procedures was used to assess hemodynamic response to negative pressure applied to the lower parts of the body (NPLB) in 56 patients with acute myocardial infarction and varying degrees of heart failure (HF) and 20 normal subjects. Normal subjects and HF-free patients showed a significant decrease in their stroke and cardiac indices and pulse pressure, and a rise in specific peripheral resistance, while the HF patients demonstrated higher cardiac productivity and lower specific peripheral resistance. Within 3 minutes after the discontinuation of NPLB, part of the depot blood returned to the central channel, creating a volumetric load on the heart. In this situation, the pump function of the heart was activated in normal subjects and HF-free patients, while patients with latent HF showed no such response, and those with obvious HF demonstrated impaired pump function.     

Enhanced resistance of the heart to arrhythmogenic factors as affected by adaptation of the body to stress exposures

Adaptation to short-term nondamaging stress effects largely limits or prevents cardiac arrhythmias in acute ischemia and reperfusion. The study examines to what extent this anti-arrhythmic effect depends on adaptational shifts of the heart itself. Isolated hearts of animals adapted to stress are shown to possess dramatically increased resistance to arrhythmias induced by local ischemia and reperfusion. The role of activated prostaglandin biosynthesis, adenosine, antioxidant systems, desensitization and other protective control systems functioning at heart level to provide this anti-arrhythmic effect is discussed.     

Ultrastructure of the heart muscle in experimental myocardial infarct following physical training

The ultrastructure of peri- and extra-infarction areas was examined in the left-ventricular myocardium of rats after swimming exercise. The ultrastructural study of cardiomyocytes and blood capillaries has suggested that regular exercise under experimental myocardial infarction improves blood supply to the heart muscle, prevents fibrillogenesis and activates compensatory-adaptive response of the intracellular regeneration type within components of the capillary wall and cardiomyocytes.