Mito KATP通道开放对重症急性胰腺炎大鼠心肌的保护作用

The Myocardial Protection of Opening MitoK_(ATP) Channel in Rats with Severe Acute Pancreatitis

目的:探讨线粒体ATP敏感性钾(MitoKATP)通道开放对重症急性胰腺炎(SAP)心肌的保护作用及机制。方法:清洁级雄性SD大鼠36只随机分为4组,K组假手术;M组建立SAP大鼠模型;D组和H组分别给予连续腹腔注射二氮嗪(DZ)、DZ+5-羟基葵酸盐(5-HD)3d后建立SAP大鼠模型。检测4组大鼠术后24h血清肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)水平;分光光度法测定心肌组织Na+-K+-ATPase活性;流式细胞仪检测心肌细胞线粒体膜电位(Δψm)变化;原位末端标记(TUNEL)法检测心肌细胞凋亡情况;留取部分心脏、胰腺组织行病理学检查。结果:M组CK-MB、LDH水平、心脏病理评分及凋亡指数较D组升高,Na+-K+-ATPase活性及Δψm较D组降低,差异均有统计学意义(P<0.01),但M组上述指标与H组比较差异均无统计学意义(P>0.05)。结论:MitoKATP通道开放对SAP引起的心肌损伤有保护作用,且上述作用可被该通道阻滞剂阻断。

Objective： To investigate the role of MitoKATP in rats with severe acute pancreatitis （SAP） and its mechanism of myocardial protection. Methods： Thirty-six healthy SD rats were randomly divided into 4 groups, sham operation group （K）, SAP rat model group （M）, consecutive intraperitoneal injection of diazoxide （DZ） group （D） and consecutive intraperitoneal injection of DZ＋5-hydroxydecanoate formate （5-HD） group （H）. The levels of serum creatine kinase isoenzyme （CK-MB） and lactate dehydrogenase （LDH） were detected 24 hours after the operation in four groups. The Na^＋K^＋-ATPase activity of myocardial tissue was detected by spectrophotometry. The alteration of mitochondrial membrane potential （△ψm） was detected by flow cytometry. The technique of TUNEL was used to detect myocardial apoptosis. Samples of heart and pancreas were stored to perform histopothological examination. Results： Compared with D group, the levels of serum CK-MB and LDH, the heart pathological scores and the myocardial apoptosis index were higher in M group （P 〈 0.01）, while the Na^＋-K＋-ATPase activity and △ψm decreased in M group （P 〈 0.01）. But there were no significant differences in above parameters between M group and H group （P 〉 0.05）. Conclusion： The opening of MitOKATP channel had myocardial protective effect in rats with SAP, which can be blocked by the channel blockers.