Kapel'ko V I, Novikova N A, Kupriianov V V, Sake V A
Fiziol Zh (1978). 1991 Nov-Dec;37(6):3-9.
The cardiac output of isolated working rat heart and left ventricular pressure were estimated in either almost complete inhibition of creatine kinase by iodoacetamide or predominant fall in adenine nucleotides (AdN) content induced by 2-deoxyglucose treatment. In the former case, a profound cardiac pump failure was observed despite almost normal levels of myocardial AdN and phosphocreatine. Those hearts could not maintain the aortic output at standard load due to lower LV systolic pressure, that was accompanied by increased minimal and maximal diastolic pressures by 5-7 mm Hg as well as by LV diastolic stiffness. As LV systolic pressure in those hearts was unchanged in retrogradely perfused and unloaded hearts it might be suggested that the cardiac pump failure was caused by the decreased LV distensibility. On the contrary, deoxyglucose treatment that resulted in 70% fall in the AdN content was accompanied by only moderate reduction of the cardiac output and insignificant changes in LV diastolic pressure and stiffness. The results suggested that creatine kinase plays a crucial role in the maintenance of normal myofibrillar compliance, which is necessary for cardiac filling and pump function.
在通过碘乙酰胺几乎完全抑制肌酸激酶或用2-脱氧葡萄糖处理导致腺嘌呤核苷酸（AdN）含量显著下降的情况下，对离体工作大鼠心脏的心输出量和左心室压力进行了评估。在前一种情况下，尽管心肌AdN和磷酸肌酸水平几乎正常，但仍观察到严重的心泵衰竭。由于左心室收缩压降低，这些心脏无法在标准负荷下维持主动脉输出，同时最小和最大舒张压升高5-7 mmHg，左心室舒张硬度增加。由于这些心脏在逆行灌注和卸载心脏时左心室收缩压不变，因此可能表明心泵衰竭是由左心室扩张性降低引起的。相反，导致AdN含量下降70%的脱氧葡萄糖处理仅伴有心输出量适度降低，左心室舒张压和硬度无明显变化。结果表明，肌酸激酶在维持正常肌原纤维顺应性方面起着关键作用，而这对于心脏充盈和泵功能是必要的。
