论文部分内容阅读
缺血-再灌注(I-R)可引起肌膜损伤、Na+/Ca2+交换逆转以及肌(内)质网钙泵(SERCA)含量或活性下降从而导致心肌钙超载。钙超载诱导心肌Calpain活化与线粒体膜通透性转换孔(mPTP)开放进而引起心肌细胞收缩功能障碍、凋亡甚至坏死。通过抑制Na+/Ca2+交换蛋白、Na+/H+交换蛋白、Calpain活性、mPTP开放、Ryanodine受体及IP3受体,或提高SERCA2a含量或活性均能显著减轻I-R心肌钙超载;采用酸性再灌注、缺血后适应与缺血预适应等措施也被证实能有效防治I-R损伤。进一步研究探索防治心肌I-R损伤策略对于缺血性心脏病的防治具有深远的意义。
Ischemia-reperfusion (I-R) can cause damage to the myofascial membrane, reversal of Na + / Ca2 + exchange and decrease in SERCA content or activity resulting in calcium overload in the myocardium. Calcium overload induces the activation of myocardial Calpain and the opening of mitochondrial membrane permeability transition pore (mPTP) which in turn leads to myocardial dysfunction, apoptosis and even necrosis. The calcium overload of IR myocardium could be significantly alleviated by inhibiting Na + / Ca2 + exchanger, Na + / H + exchanger, Calpain activity, mPTP opening, Ryanodine receptor and IP3 receptor, or increasing SERCA2a content or activity. Post-conditioning and ischemic preconditioning and other measures have also been proven to effectively prevent IR injury. Further research to explore the prevention and treatment of myocardial I-R injury strategy for the prevention and treatment of ischemic heart disease has far-reaching significance.