目的:探讨大鼠心肌细胞缺氧预处理(IPC)时线粒体KATP+通道的作用及其与P38MAPK、INOS和COX -2的关系。方法:实验分为8组(对照组、缺氧预处理组、IPC+HOPR组、IPC+HDPO组、DZX+SB组、DZX+SMT组、 DZX+NS组和DZX+HD组),用WESTERN BLOTTING法测定心肌细胞的COX-2、INOS表达量和PHOSPH-P38MAPK量,以 LDH释放和台盼蓝排斥试验判断心肌细胞损伤程度。结果:IPC前加入5-HD能抑制P38MAPK、INOS和COX-2 表达,并能取消IPC的心肌保护作用;IPC及二氮嗪预处理后加入5-HD不抑制P38MAPK、INOS和COX-2表达,但也取消IPC的心肌保护作用。二氮嗪预处理后加入SB203580能抑制INOS和COX-2表达;加入SMT能抑制COX- 2表达但不抑制INOS表达;加入NS398不抑制P38MAPK和INOS表达。结论:IPC晚期保护作用中,线粒体KATP+通道发挥了双重作用,既是P38MAPK、INOS和COX-2上游触发子,又是IPC后期的效应子。 AIM: To investigate the role of mitochondrial KATP + channel in rat cardiomyocytes under hypoxic preconditioning (IPC) and its relationship with P38MAPK, INOS and COX-2. Methods: The experiment was divided into 8 groups (control group, hypoxic preconditioning group, IPC + HOPR group, IPC + HDPO group, DZX + SB group, DZX + SMT group, DZX + NS group and DZX + HD group) BLOTTING method was used to determine the expression of COX-2, INOS and PHOSPH-P38MAPK in cardiomyocytes. LDH release and trypan blue exclusion test were used to determine the extent of cardiomyocyte injury. Results: IPC pretreatment with 5-HD inhibited the expression of P38MAPK, INOS and COX-2, and abolished IPC cardioprotection. IPC and diazoxide pretreatment did not inhibit the expression of P38MAPK, INOS and COX-2 , But also to cancel the myocardial protection of IPC. Addition of SB203580 after diazoxide pretreatment inhibited INOS and COX-2 expression; addition of SMT inhibited COX-2 expression but did not inhibit INOS expression; addition of NS398 did not inhibit P38MAPK and INOS expression. Conclusions: Mitochondrial KATP + channels play a dual role in the protective effect of IPC, which is not only the upstream of P38MAPK, INOS and COX-2 but also the effector of IPC.