[Effect of sodium oxybutyrate on macroergic phosphates, function and ultrastructure of the myocardium in blood loss].
Experiments on dogs with long-term hypotony caused by blood loss have demonstrated irreversible lesions in the majority of cardiomyocytes and hypodynamic condition of the heart with a high content of macroergic phosphates in the myocardium. Intravenous injection of sodium hydroxybutyrate in a dose of 180-200 mg/kg after 60 min of hypotony seems to improve energy transport and utilization in the ischemic myocardium. It increases the working capacity and power of the heart muscle, pump function of the heart and makes longer the period of ultrastructural changes in cardiomyocytes.
D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003401:Creatine / Q000378:metabolism; D004285:Dogs; D004734:Energy Metabolism / Q000187:drug effects*; D006321:Heart / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects; D006470:Hemorrhage / Q000503:physiopathology*; D006885:Hydroxybutyrates / Q000494:pharmacology*; D007022:Hypotension / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D010725:Phosphocreatine / Q000378:metabolism; D012978:Sodium Oxybate / Q000494:pharmacology*
D006885:Hydroxybutyrates; D010725:Phosphocreatine; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D012978:Sodium Oxybate; D000255:Adenosine Triphosphate; D003401:Creatine
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