Effect of urocortin I pretreatment on heart function and ATP in rat heart during myocardial ischemia-reperfusion injury

LIU Wei; GU Yan; TIAN Wei; ZHANG Lin; LI Jia; DENG Shengli

doi:10.3969/j.issn.1006-5725.2017.18.011

Abstract：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 N1),ischemia-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 min ,group IR experienced 40 min ischemia and 60 min reperfusion ,group U1 received urocortin I for 30 min before ischemia,and group HU1 received 5-HD for 5 min 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 myocardium were evaluated. Part Ⅱ. The isolated and cultivated myocytes were randomly divided into four groups:group N2,HR,U2 and HU2. 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 min 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 mitoKATP channel,thus maintaining the microstructures of myocytes and improving heart function after ischemia-reperfusion injury.