通过增加“钙反常”及缺血后再灌注时的人工跨膜钠梯度预防心肌再灌注损伤
[Prevention of myocardial reperfusion injury by increasing artificial trans-membrane sodium gradient in "calcium paradox" and post-ischemic reperfusion].
作者信息
Alabovskiĭ V V, Vinokurov A A, Kobrin V I, Oleĭnikov O D
出版信息
Fiziol Zh (1978). 1991 May-Jun;37(3):25-30.
An effect of the high sodium gradient during "calcium paradox" and postischemic reperfusion has been studied. A decrease of Na/Ca exchange by high sodium gradient (200 mM NaCl in the perfusion solution) resulted in the reduction of myoglobin release from the heart during "calcium paradox". High sodium concentration solution (200 mM) increased protective effect of ATP during "calcium paradox". Exogenous phosphocreatine (100 mumol/mol) increased myoglobin release from the heart. During perfusion of the heart by high sodium concentration, phosphocreatine efficiently decreased myoglobin release from the heart during "calcium paradox". Exogenous ATP (as Na-pump activator) and high Na+ concentration solution (180 mM) prevented the LDH release from the myocardium, decreased ATP hydrolysis, inhibited Ca influx, maintained total adenine nucleotides, phosphate potential, energy charge of the cardiomyocytes.
研究了“钙反常”和缺血后再灌注期间高钠梯度的作用。高钠梯度（灌注液中200 mM NaCl）导致钠/钙交换减少，从而在“钙反常”期间使心脏肌红蛋白释放减少。高钠浓度溶液（200 mM）在“钙反常”期间增强了ATP的保护作用。外源性磷酸肌酸（100 μmol/mol）增加了心脏肌红蛋白的释放。在高钠浓度灌注心脏期间，磷酸肌酸在“钙反常”期间有效减少了心脏肌红蛋白的释放。外源性ATP（作为钠泵激活剂）和高钠浓度溶液（180 mM）可防止心肌中乳酸脱氢酶的释放，减少ATP水解，抑制钙内流，维持心肌细胞的总腺嘌呤核苷酸、磷酸势和能量电荷。
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