[Nucleic acid metabolism in the myocardium and their content in the blood in experimental myocardial infarct]. / Obmen nukleinovykh kislot v serdechnoi myshtse i ikh soderzhanie v krovi pri éksperimental'nom infarkte miokarda.

Significant shifts were revealed in the content, disintegration, and synthesis of nucleic acids in the zone of the infarction and adjacent areas of the heart in experiments on 83 dogs. In the area of the necrosis, the total level and RNA transformation are reduced at the beginning but grow with the development of the reparative processes, whereas DNA metabolism is activated stably beginning with the 1st day of the reproduction of the pathological condition. Short-term changes in nuclein metabolism, similar to those in the zone of the infarction, occur in the adjacent areas. In myocardial infarction, in the initial stage of its development too, the heart does not secrete nucleic acids or polynucleases into the coronary sinus and their values in the serum are close to normal. Long-term activation of deoxyribonuclease in myocardial infarction is the cause of the stable increase in the blood of the products of DNA hydrolysis, which is recommended as a pathogenetically substantiated laboratory diagnostic test for this disease.

[Possible metabolic mechanisms of coronary circulatory disorder in an intact area of the left ventricle in experimental myocardial infarct]. / Vozmozhnye metabolicheskie mekhanizmy narusheniia koronarnogo krovoobrashcheniia v intaktnoi zone levogo zheludochka serdtsa pri éksperimental'nom infarkte miokarda.

In dogs with experimental myocardial infarction the anterior descending branch of the left coronary artery was ligated and 1, 2, 3, 5, and 10 days later its circumflex branch was catheterized and perfused, and coronary circulation in the intact myocardial zone, systemic hemodynamics, the AMP content and the activity of enzymes catalysing adenosine metabolism were studied. In the intact myocardial zone resistance increases in the coronary vessels and neurohumoral regulation is disturbed, the beta-adrenergic and cholinergic reactions of dilation are weakened, alpha-adrenergic pressor effect of catecholamines on the cardiac vessels is manifested, and adenosine metabolism is disturbed. Disorders of adenosine metabolism are regarded among the possible mechanisms of coronary circulatory disorders in the intact zone of the myocardium.

[Adenosine metabolism in the myocardium in experimental myocardial infarct]. / Obmen adenozina v serdtse pri eksperimental'nom infarkte miokarda.

It was shown in dog experiments that the formation and content of the adenosine precursor in the zone of the infarction and the surrounding parts of the myocardium undergo no essential changes. At the same time, further conversion of adenosine monophosphate in an infarction heart is deeply disturbed due to shifts in the enzymatic systems of the adenosine cycle. In the area of the necrosis adenosine monophosphate is metabolized mainly without the production of adenosine because high activity of AMP aminohydrolase here occurs in conjunction with deep inhibition of 5-nucleotidase. Diametrically opposite relationships are created in the myocardium outside of the focus of infarction and adenosine production does not suffer evidently. In both areas of the involved heart adenosine decomposition is delayed due to the inhibition of adenosine deaminase, but in the infarction zone this shift is restricted to 48 hours whereas in the periinfarction zone it is not corrected even 10 days after reproduction of the pathological condition.

Protein and polynucleotide metabolism in skeletal muscles in dogs with experimental myocardial infarction.

In experiments on 105 dogs it was found that at the onset and in the course of extensive myocardial infarction there regularly occur a specific set of shifts in the protein and nuclein metabolism in skeletal muscles. Besides changes reflecting a certain decrease in the functional capacity of muscles there also appear metabolic reactions of compensatory nature. Changes in nitrogen metabolism in striated muscles are most pronounced in the formation period of myocardial infarct but partially persist during the organization stages, some of them up to a period of a whole month. The intensities of changes are mostly expressed by values 20-35% higher than the initial ones, but in some indicators the alterations are still more intense.

[Changes in the metabolism of adenine-containing components in the heart during experimental myocardial infarct]. / Izmeneniia obmena adeninsoderzhashchikh komponentov v serdtse pri éksperimental'nom infarkte miokarda.

Turnover of heart polynucleotides, adenine nucleotides and adenosine was studied in dynamics of dog experimental myocardial infarction. In the areas of necrosis an inhibition of RNAase and DNAase was observed and later on - an activation of these enzymes with simultaneous increase in content of RNA and DNA; the stable decrease in ATP and ADP content was also found but content of AMP remained at the initial level. Conversion of AMP into adenosine was limited due to inhibition of 5-nucleotidase, whereas the direct AMP deamination and degradation of adenosine proceeded with the normal rate. Out of the necrosis area 5-nucleotidase maintained the high activity but both "non-adenosine" pathway of AMP degradation and adenosine splitting were inhibited; this promoted the nucleoside formation and maintained its level in the tissue. Alterations in content of RNA, DNA and adenine mononucleotides out of the infarction area were similar to the alterations in the impaired zone but less distinct and stable.

[Effect of heparin on nitrogen metabolism in the myocardium of dogs under normal conditions and following an experimental myocardial infarct]. / Vplyv heparynu na azotystyi obmin u sertsevomu m'iazi sobak u normi ta za eksperymental'noho infarktu miokarda

Heparin administered at the initial stage of myocardium infarction is shown to prevent a number of shifts in the metabolism of protein and polynucleotides of the injured heart. It does not promote the development of some changes, but intensifies only a few of those evoked by the ligation of coronary artery in the myocardium nitrogen metabolism. The preparation inhibitory effects are also slightly pronounced in the normal myocardium where the preparation activates many metabolic reactions of nitrogen-containing biopolymers. Inactivation of enzymatic systems in a cell is likely to be not the basic, as some researchers consider, but one of the secondary mechanisms of heparin incorporation into metabolism proceeding in normal and pathologically changed tissues.

[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.

[Certain nitrogen-containing components of the heart, of the coronary-sinus blood and of the aorta in experimental myocardial infarct]. / Nekotorye azotsoderzhashchie komponenty serdtsa, krovi koronarnogo sinusa i aorty pri eksperimental'nom infarkte miokarda

Forty-two dogs were subjected to studies of nitrogen-containing metabolites in the blood of the aorta, coronary sinus and in various parts of the heart under normal conditions and 1, 24 hours and 3 days following the induction of myocardial infarction. In normal dogs the myocardium usually retains from the in-flowing blood such components as urea, glutamine, RNA, non-organic phosphates, while the arterio-venous gradient of ammonium, DNA and nucleases is close to zero. The ligation of the coronary sinus is followed by a deceleration of urea formation in the liver, the amount of urea formation in the liver, the amount of urea in the arterial blood and myocardium decreases, the latter, instead of retaining it, throwing it out into the coronary sinus. Like in normal cases, in this pathology the heart muscle is capable of synthesizing urea from ammonium. The infarctized heart actively retains glutamine from blood using it in situ, and does not increase the secretion of free ammonium into the coronary sinus. The level of nucleic acids and the activity of the nucleases significantly increase in the diseased tissue, undergoing no important changes in the blood circulating in the cardiac vessels.

Fractional composition and metabolism of proteins, and levels of polynucleotides, in canine heart in experimental myocardial infarction.

In 108 dogs, experimental infarction of the left ventricular anterior wall was produced by ligation of the descending branch of left coronary artery, and the myocardium was tested for the total content, fractional composition, and metabolism of proteins as well as for the levels of nucleic acids. The most profound metabolic changes were found in the necrotic zone, where there occur an irreversible decrease in the content of soluble proteins, an accumulation of stromatic fractions, and an inhibition of fundamental reactions of nitrogen metabolism; during the period of organization of the infarct, the ribonucleic acid level steeply rises. In the intact left ventricular segment there occur changes analogous to those in the infarcted zone, but less intense; such changes combine with some alterations of rather compensatory nature, which, however, are characteristic of those myocardial segments in which the coronary circulation has not been disturbed.