Urocortin Ⅰ预处理对缺血再灌注损伤鼠心心功能及细胞ATP含量的影响  

Effect of urocortin Ⅰ pretreatment on heart function and ATP in rat heart during myocardial ischemiareperfusion injury

作　　者：刘为[1] 顾燕[2] 田伟 张琳[1] 李佳[4] 邓胜利[4] 

机构地区：[1]遵义医学院麻醉学系,贵州省麻醉与器官重点保护实验室,563000 [2]重庆市妇幼保健院麻醉科,400010 [3]遵义市播州区人民医院麻醉科,563000 [4]遵义医学院附属医院麻醉科,563000

出　　处：《实用医学杂志》2017年第18期3021-3025,共5页The Journal of Practical Medicine

基　　金：贵州省科学技术基金资助项目(编号:黔科合J字[2008]2196)

摘　　要：目的探索Urocortin Ⅰ预处理对缺血再灌注损伤鼠心心功能及细胞ATP含量的影响。方法实验一:48只SD大鼠随机分为4组(n=12):正常组(N_1组)、缺血再灌注组(IR组)、Urocortin Ⅰ预处理组(U_1组)、5-羟葵酸(5-HD)+Urocortin Ⅰ组(HU_1组)。N_1组平衡灌注155 min;IR组缺血40 min后复灌60min;U_1组缺血前给予Urocortin Ⅰ 30 min;HU_1组Urocortin Ⅰ预处理前给予5-HD 5 min。观察各组鼠心心率(HR)、左室发展压(LVDP)、左室舒张末压力LVDEP及左心室内压力最大上升速率dp/dt(dp/dt_(max))及超微结构的变化。实验二:将分离培养后的心肌细胞随机分为正常组(N_2组)、缺氧复氧组(HR组)、Urocortin Ⅰ预处理组(U_2组)、5-HD+Urocortin Ⅰ组(HU_2组)。除N_2组持续培养155 min外,余各组均缺氧40 min后复氧60 min。U_2组缺氧前给予Urocortin Ⅰ 30 min;HU_2组Urocortin Ⅰ预处理前给予5-HD 5 min。于复氧末检测心肌细胞ATP含量。结果 Urocortin Ⅰ预处理能抑制缺血再灌注损伤引起的HR、LVDP、dp/dt的下降及LVEDP的升高,并能保存缺氧复氧心肌细胞ATP的含量,维持心肌超微结构的稳定。结论 Urocortin Ⅰ不仅可增强离体鼠心心脏收缩功能,而且可通过开放mitoK_(ATP)保存心肌细胞ATP含量,保护心肌细胞超微结构,改善缺血再灌注后的心脏功能。Objective To investigate the effect of Urocortin I pretreatment on heart function and ATP in rat heart during myocardial ischemia-reperfusion injury. Methods Part I. 48 SD rats were randomly divided into four groups （n=12） ： normal group （group N, ）, isehemia-reperfusion group （group IR）, urocortin I pretreatment group （group U1） , and 5-HD＋urocortin I group （group HU1）. Group N1 received continuous perfusion for 155 rain, group IR experienced 40 min isehemia and 60 rain reperfusion, group UI received urocortin I for 30 rain before ischemia, and group HU1 received 5-HD for 5 rain before urocortin Ⅰ pretreatment. Changes of heart rate （HR） , left ventricular end-diastolic pressure （LVEDP） , left ventricular developed pressure （LVDP） , maximum dp/dt （dp/dtmax） and microstructure of myoeardium were evaluated. Part Ⅱ. The isolated and cultivated myocytes were randomly divided into four groups： group N2, HR, U2 and HU〉 Group N2 was cultured continuously for 155 min, while other groups experienced 40 min-anoxia and 60 min reoxygenation. Urocortin I was added to group U2 for 30 rain before anoxia. 5-HD was added to group HU2 before adding urocortin I. The content of ATP at the end of reoxygenation was detected. Results Urocortin I pretreatment restrained the decline in HR, LVDP, and dp/dt and the rise in LVEDP during ischemia-reperfusion injury. Furthermore, the content of ATP was preserved and the microstructure of myocardium was sustained during anoxia/reperfusion. Conclusions Urocortin I pretreatment can not only enhance cardiac contractility of the isolated heart, but also preserve the content of ATP through the opening of mitoKA.re channel, thus maintaining the mierostructures of myocytes and improving heart function after ischemia-reperfusion injury.

关 键 词：UROCORTIN I 预处理 缺血再灌注 ATP 心功能 

分 类 号：R541[医药卫生—心血管疾病]