[Molecular mechanisms of cardiac insufficiency in myocardial ischemia].
An analysis of the main concepts of the pathogenesis of heart muscle insufficiency under ischaemia was conducted. None of the hypotheses postulating the invariability of the energy supply to the myofibrills was shown to explain the fast reduction of the contractility of the ischaemic myocardium. These hypotheses are based on the experimental fact of the ATP level in the myocardium practically undergoing no reduction under ischaemia. At the same time, one of the earliest changes in the heart muscle under ichaemia consists in creatine phosphate concentration reduction that correlates with the decrease in the contractility. The recently obtained data indicate that the energy synthesized in the mitochondria of the cardiac muscle is carried away from them in the form of energy of creatine phosphate molecules that is later used for ATP synthesis in the myofibrill creatine phosphokinase reaction. A scheme is suggested that implies that under ischaemia severe changes in the energy supply consisting in creatine phosphate synthesis reduction are the leading factor in the pathogenesis resulting on the early stages of the process in a reduction of the contractility, and on the later ones--in irreversible damages of the membrane systems and cell destruction.
D000255:Adenosine Triphosphate / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D003327:Coronary Disease / Q000503:physiopathology*; D004734:Energy Metabolism; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008931:Mitochondria, Muscle / Q000378:metabolism; D008954:Models, Biological; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology; D009210:Myofibrils / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism
D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D002118:Calcium
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