Ventura-Clapier R, Veksler V K, Elizarova G V, Mekhfi H, Levitskaya E L, Saks V A
Physiologie Cellulaire Cardiaque, INSERM U-241, Université Paris Sud, Orsay, France.
Biochem Med Metab Biol. 1987 Dec;38(3):300-10. doi: 10.1016/0885-4505(87)90094-6.
After prolonged ischemia followed by reperfusion of the isolated rat heart, irreversible heart failure is associated with creatine kinase leakage from the cells. The possible implications of MM creatine kinase leakage from myofibrillar compartments on the contractile properties of ventricular muscle have been studied in control versus ischemic hearts. Total creatine kinase activity decreased in ischemic cells while creatine kinase and ATPase activities were not modified in isolated myofibrils. The efficiency of creatine kinase and phosphocreatine in the relaxation of rigor tension in skinned ventricular preparations was not changed after ischemia. Furthermore, neither the pCa/tension relationship nor the rate of tension development following length changes were modified by ischemia. These results show that the contractile properties of myofilaments as well as the functional coupling between myosin ATPase and creatine kinase are preserved in ischemic hearts suffering irreversible contractile failure.
在离体大鼠心脏经历长时间缺血后再灌注,不可逆性心力衰竭与肌酸激酶从细胞中漏出有关。已在对照心脏与缺血心脏中研究了肌酸激酶MM从肌原纤维区室漏出对心室肌收缩特性的潜在影响。缺血细胞中的总肌酸激酶活性降低,而分离出的肌原纤维中的肌酸激酶和ATP酶活性未改变。缺血后,在去表皮心室标本中,肌酸激酶和磷酸肌酸缓解强直张力的效率没有变化。此外,缺血并未改变pCa/张力关系,也未改变长度变化后张力发展的速率。这些结果表明,在遭受不可逆收缩功能衰竭的缺血心脏中,肌丝的收缩特性以及肌球蛋白ATP酶与肌酸激酶之间的功能偶联得以保留。