复苏后心功能障碍是影响复苏预后的重要环节，其机制不同于其他局部心肌缺血再灌注模型，但其机制尚不清楚，也缺乏有效治疗手段。本研究团队的前期研究结果提示肌浆网—线粒体单位Ca2+调控蛋白损伤和心肌细胞间连接蛋白Cx43损伤是其中的两个关键环节。总结一国外最新相关研究和我们的前期研究的基础上推测，PI3K-Akt-NO及相关信号通路可能在上述损伤过程中发挥重要的调控作用，并可能具有减轻骤停—复苏和复苏后早期两个阶段心肌损伤的潜在可能。本研究拟在心肺复苏模型中，采用各种基因干预技术或药物干预PI3K、Akt、NO及各下游激酶的表达及活性，采用各种分析和检测方法，从骤停—复苏和复苏后早期两个阶段，从系统、细胞和分子水平全面研究PI3K-Akt-NO信号通路在复苏中通过调控肌浆网、线粒体损伤和心肌细胞间连接蛋白损伤从而改善复苏后心功能，并深入探索上述过程的相关蛋白靶点和分子机制。

Postresuscitation myocardial dysfunction is related to the mortalty of patients who survived from initial resuscitation. Our previous study have shown that the abnormalities of of sarcoplasma-mitochondrial unit Ca2+ handling proteins and myocardial connexin 43 play an essential role in the mechanisms of postresuscitation myocardial dysfunction. Furthermore, it is suggested that PI3K-Akt-NO signaling pathway might have the potential to modulate these pathological process during arrest-CPR phase and early phase postresuscitation. In the present study, we plan to investigate whether the modulation of PI3K-Akt-NO pathway can improve postresuscitation myocardial dysfunction by modulating the function of sarcoplasma-mitochondrial unit Ca2+ handling proteins and myocardial connexin 43 protein during arrest-CPR phase and early phase postresuscitation.The involvement of relevant proteins and signaling pathways wll also be studied.