[Evaluation of cardiac function in patients with ischemic heart disease in the early stages of controlled physical exercise]. / Otsenka funktsional'nogo sostoianiia seratsa u bol'nykh ishemicheskoi bolezn'iu serdtsa na rannykh étapakh dozirovannoi fizicheskoi nagruzki.

Fifty-nine coronary patients and 20 clinically normal subjects were investigated. Coronarography was performed in 21 patients. Everybody was referred to one of the three functional classes. Central hemodynamic parameters were measured using tetrapolar chest rheography. Venous levels of lactic and pyruvic acids were also measured. The measurements were taken in resting conditions and under threefold increase in systemic oxygen consumption following bicycle ergometry in supine position. Three types of response were identified: normal, compensated and decompensated ones. On the basis of these, functional reserves of the heart can be evaluated at earlier stages of rationed exercise, this being particularly important for coronary patients not to be exposed to maximum and submaximum physical stress.

[Relationship between anaerobic energy formation and myocardial contractile function in disturbed cardiac blood supply]. / Zavisimost' mezhdu anaérobynym énergoobrazovaniem i sokratitel'noi funktsiei miokarda pri narushenii krovsnabzheniia serdtsa.

Graded 70 and 90% restrictions of the coronary blood flow were reproduced in dogs with closed chest upon catheterization and autoperfusion of the circumflex branch of the left coronary artery. Interrelations between shifts in anaerobic carbohydrate metabolism and the main parameters of myocardial contractility were explored. An increase in glycolytic and phosphorylase activities, lactic acid concentration and a drop in the glycogen level were disclosed. The alterations were most pronounced in the ischemic area upon 90% restriction of coronary perfusion, whereas in the left ventricular myocardium outside the ischemic area, they were less detectable. There was a significant negative correlation between the lactate level and glycolysis intensity in both the heart areas under study and the contractility rate parameters dp/dt max, Vpm. dp/dt/p, etc. Lactic acid accumulation in the ischemic myocardium is an important factor inhibiting contractility. This may be caused by acidosis as well as by the mechanisms which are independent of pH changes.

[Myocardial carbohydrate metabolism in limited coronary blood flow]. / Uglevodyni obmen miokarda pri ogranichenii koronarnogo krovotoka.

Dosaged restriction of coronary blood flow (by 30, 50, 70 and 90%) was reproduced for 30 minutes in dogs with a closed chest. In all degrees of coronary blood flow restriction the loss of glycogen, accumulation of lactic acid and cAMP (in reduction of blood flow by 50 and 70%) and activation of glycogenolysis, phosphorylase and phosphofructokinase were recorded in the zone of ischemia. The changes advanced with the deepening of ischemia. Similar, though less pronounced changes were found outside the ischemic zone. Marked metabolic shifts were disclosed in the right ventricle. The mechanisms of anaerobic oxidation activation in ischemia are discussed.

[Energy formation processes in the myocardium during measured limitation of coronary blood flow]. / Protsessy énergoobrazovaniia v miokarde pri dozirovannom ogranichenii koronarnogo krovotoka.

Effect of short-term partial limitation of coronary circulation (by 30%, 50% and 70%) on energy formation in myocardium was studied in animals with closed thorax after catheterization and autoperfusion of the circumflex branch of left coronary artery. Distinct alterations in energy metabolism were observed already after a decrease of the coronary circulation by 30%. Several enzymes were inhibited in tricarboxylic acid cycle and in respiratory chain following development of ischemia. Despite of the inhibition of the aerobic oxidation content of ATP and glycogen maintained rather stable. Content of ATP was decreased down to 60% of the initial level only after limitation of the circulation by 2/3. Deficiency in aerobic energy production as well as maintaining of a rather stable content of ATP and glycogen were apparently compensated by an increase in cAMP content, activation of glycolysis and pentose phosphate pathway and of adenosine formation.

[Metabolic shifts in acute period of myocardial infarct and the possibility of their correction with curantil]. / Metabolicheskie sdvigi v ostrom periode infarkta miokarda i vozmozhnosti ikh korrektsii s pomoshch'iu kurantila.

The effect of curantil on the values of energy metabolism in different parts of the myocardium was studied on dogs with experimental myocardial infarction. Tissue respiration, the activity of Krebs' cycle enzymes, cytochrome oxidase, pentose phosphate cycle and glycolysis, and the content of glycogen and adenyl components were studied. It was established that curantil has a positive effect on energy processes, particularly in myocardial areas not involved in ischemia. It is suggested that activation of tissue oxidation enzymes, which improves oxygen utilization and increases ATP production, is among the mechanisms of the curantil effect. It is noted that curantil stimulates the synthesis of glycogen and inhibits its decomposition. The accumulation in the myocardium of AMP, the precursor of adenosine possessing a marked coronarolytic effect, is an important aspect of the drug's action.

[Serum and myocardial enzyme activity in experimental myocardial infarct]. / Aktivnost' fermentov serdechnoi myshtsy i syvorotki krovi pri éksperimental'nom infarkte miokarda

In 150 canine experiments it has been established that in myocardial infarction the activity of heart muscle enzymes decreases significantly and persistently in the zone of necrosis, moderately and reversibly--beyond this zone, individual enzymes being unequally sensitive to the effects of the given injuring factor. The shifts in the activity of the serum and heart muscle enzymes correlate only in the early days following the reproduction of the pathological state, while the levelling of hyperenzymia is accompanied by an enhancement of the enzymatic disorders in the myocardium in cases of infarction.