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急性缺血后心力衰竭可能与高能化合物的合成障碍有关.用?Wistar大鼠进行离体心脏实验,30min全心缺血和30 min再灌注导致心肌收缩力显著下降,三磷酸腺苷含量不足和线粒体内钙含量升高 用钌红(1μmol·L~(-1))进行再灌注,线粒体内钙超负荷减轻,同时心肌收缩力增加,但三磷酸腺苷含量不变 用钌红,核糖(1mmol·L~(-1))和腺嘌吟(1mmol·L~(-1))同时进行再灌注,不但心肌收缩力显著升高,而且三磷酸腺苷含量显著恢复。实验表明,急性缺血后的心肌受线粒体内钙含量升高的影响,合成高能化合物的能力减低.钌红,核糖和腺嘌吟可协同性地提高心肌肉三磷酸腺苷含量和恢复心肌收缩力。
After acute ischemic heart failure may be related to the synthesis of high energy compounds obstacles.Wistar rat heart experiments in vitro, 30min ischemia and 30min reperfusion resulted in significantly decreased myocardial contractility, ATP deficiency and mitochondrial calcium Reperfusion with ruthenium red (1μmol·L -1) increased mitochondrial calcium overload and myocardial contractility increased, but the content of adenosine triphosphate was unchanged with ruthenium red and ribose (1mmol·L -1) 1) and adenine (1mmol·L -1) at the same time reperfusion, not only significantly increased myocardial contractility, and significant recovery of adenosine triphosphate content. Experiments show that acute myocardial ischemia after myocardial mitochondrial calcium content increased the ability to synthesize high-energy compounds reduced ruthenium red, ribose and adenine can synergistically increase myocardial ATP content and restore myocardial contractility.