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|Title:||New insights in to the treatment of myocardial infarction|
|Citation:||New insights in to the treatment of myocardial infarction / Petr Sarapultsev, Oleg Chupakhin, Alex Sarapultsev, Maxim Rantsev, Larisa Sidorova, Svetlana Medvedeva, Irina Danilova // International Journal of Experimental Pathology. — 2012. — Vol. 93. — № 1. — P. 18-23.|
|Abstract:||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. © 2012 The Authors. International Journal of Experimental Pathology © 2012 International Journal of Experimental Pathology.|
|Appears in Collections:||Научные публикации, проиндексированные в SCOPUS и WoS CC|
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|10.1111-j.1365-2613.2011.00794.x.pdf||240,6 kB||Adobe PDF||View/Open|
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