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This study investigated the effects of the L-17 compound of the group of substituted 5R1, 6H2-1,3,4-thiadiazine-2-amines on the inflammatory cellular infiltration and myocardial remodelling which occurs after acute myocardial infarction (MI) in rats. The study is based upon recent clinical and experimental work which demonstrated the role of local and systemic inflammatory reactions in postinfarction remodelling. Acute MI in rats was induced by left coronary artery coagulation. Animals were sacrificed on day one, five and seven after MI induction. The myocardiumal samples were taken from all parts of the heart and examined by histology. This included areas of infarction, infraction and areas that were peri-infarctiom and left ventricular areas distant from the damaged tissues. Serum activity of creatine phosphokinase (CPK), aspartate aminotransferase (AST), isoenzymes 1 and 2 and lactate dehydrogenase (LDH1-2) were investigated on the same three days, before and in the process of MI development was investigated (at days 1, 5 and 7). The L-17 compound to not only decreased the area of initial infarction but also changed the pattern of inflammatory reaction in the affected myocardium fundamentally. Laboratory studies of effects of L-17 compound on the development and course of experimental MI showed that administration decreased blood AST and CPK levels significantly and provided useful the data about the correlation between the activity of these enzymes and the dimensions of the significantly necrotic area. In this model of experimental MI the use of the L-17 compound induced led to the replacement of the exudative destructive inflammation that is seen under standard conditions with a more cellular "productive" pattern of inflammation, with associated reduction in initial necrosis area and the, decrease in myocardial ischaemia and reperfusion injury may account for the accelerated repair process.

It is reputed that the ideal therapeutic approaches to treatment of patients with acute coronary syndrome (ACS) and myocardium infarction (MI) should be aimed at the inflammation reaction triggers. This study investigated the effectiveness of the impact of L- 17 compound of the group of 5- phenyl substituted-6H-1,3,4-thiadiazine-2-amines upon the course of experimental MI as compared to the impact of a preparation, officially registered in Russia as an immunomodulator, Tamerit, belonging to phthalhydrazid derivative substance. Acute MI in rats was induced by left coronary artery coagulation. Histological study of the myocardium sections and biochemical analysis has been carried out at the 1st and 7th days of the experimental MI. The conducted investigations have shown that under the action of immunocorrectors the inflammation reaction character changes, exudative/destructive inflammation is replaced by a proliferative-cellular one. Animals' blood biochemical analysis at the background of L-17 and Tamerit introduction has shown a decrease of aminotransferases and lactatedehydrogenases activity in blood as compared to the reference group of animals' indicators, which is evidently caused by epicardial injury of myocardium and lesser amount of the alternative cardiomyocytes. At the same time, no noticeable difference in biochemical characteristics in groups, having been treated to immunomodulators of different chemical composition was identified, which is the sign of the essential similarity of their impact. Thus, immunocorrectors of different chemical groups (Tamerit and compound L17) diminish the volume of initial myocardial infarction and accelerate the granulation processes in course of MI, and represent a new category of treatment agents.

The purpose of this study was to determine the specific features of the morphological restructuring of the myocardium in the early stage of experimental diabetes mellitus (DM). Experimental type 1 DM rat model was developed by intraperitoneal injection of alloxan solution at a dose of 30 mg per 100 g body mass. After 1 month, 3 mL of blood was drawn by heart puncture and the plasma separated by centrifugation for biochemical analysis. Plasma glucose, insulin, and glycosylated haemoglobin in whole blood were determined. Light microscopy and morphometric studies were conducted of histological slices of the hearts of experimental animals. The investigation of heart morphology showed a statistically significant alteration in chamber wall thickness in the right auricle in rats with alloxan-induced DM. A change in cardiomyocyte diameter in myocardium slices was observed in all chambers of DM rats except for the left ventricle. Average cardiomyocyte diameter in rats with experimental DM increased by 26.6% and 15.5% in the right auricle and right ventricle, respectively, while average cardiomyocyte diameter in the left auricle decreased by 20.8%. Histological investigation of the heart following alloxan injection demonstrated, under the epicardium, distended vessels of the venous collecting microcirculatory system. Aggregation and agglutination of red blood cells and endothelial cell destruction were found in some vessels. In the early stage of DM development, structural alterations in the microcirculatory channels and myocardiocytes can be observed in the heart. These structural alterations were most evident in the right chambers of the heart. Anat Rec, 298:396-407, 2015Rec, 298:396-407, . V C 2014 Wiley Periodicals, Inc.

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