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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 preconditioning on cardiac function and cellular ATP content in rats with ischemia-reperfusion injury. Methods Experiment 1: 48 SD rats were randomly divided into 4 groups (n = 12): normal group (N 1 group), ischemia reperfusion group (IR group), Urocortin Ⅰ pretreatment group (U_1 group) (5-HD) + Urocortin Ⅰ group (HU_1 group). Rats in group N_1 were given perfusion for 155 min. Rats in IR group were reperfused for 60 min after 40 min of ischemia. Urocortin Ⅰ was given for 30 min before ischemia in U_1 group and 5-HD for 5 min before pretreatment in group HU_1. The changes of heart rate (HR), left ventricular development pressure (LVDP), left ventricular end-diastolic pressure (LVDEP) and left ventricular pressure maximum dp / dt max (dp / dt max) and ultrastructure were observed. Experiment 2: The isolated cardiomyocytes were randomly divided into normal group (N 2 group), hypoxia-reoxygenation group (HR group), Urocortin Ⅰ pretreatment group (U_2 group), 5-HD + Urocortin Ⅰ group ). Except N_2 group cultured continuously for 155 min, the remaining groups were reoxygenated for 60 min after 40 min of hypoxia. U2 group were given Urocortin Ⅰ for 30 min before hypoxia; 5-HD for 5 min before Urocortin Ⅰ pretreatment in HU2 group. At the end of reoxygenation, the ATP content in cardiomyocytes was measured. Results Pretreatment with Urocortin Ⅰ could inhibit the decrease of HR, LVDP, dp / dt and LVEDP induced by ischemia-reperfusion injury and maintain the content of ATP in hypoxia-reoxygenation cardiomyocytes and maintain the ultrastructure of myocardium. Conclusions Urocortin Ⅰ not only enhances cardiac systolic function in isolated rat hearts, but also protects cardiomyocytes ultrastructure and improves cardiac function after myocardial ischemia-reperfusion by opening ATP mitochondria ATP content.