【Abstract】

Objective To study the protective effect of hyperpolarized cardioplegic arrest on reperfused rat heart perfermance and to investigate the role of mitochondrial KATP opening against ischemia/reperfusion damage.

 Methods Sprague-Dawley (SD) rats weighing 250-350g were randomly divided into five groups (8 rats each group): control (group C), depolarized arrest (group D), hyperpolarized arrest (group H), depolarized arrest plus adding 5-HD (group 5HD+D) and hyperpolarized arrest plus 5-HD (group 5HD+H). Hearts in each group were subjected to global ischemia at 37℃ for 40 min followed by 30 min reperfusion after a 20-minute equilibration period. Left ventricular developed pressure (LVDP), Left ventricular end diastolic pressure (LVEDP),heart rate (HR) and coronarary flow (CF) were determined to measure the recovery of the myocardial performance after 30-min reperfusion; Before ischemia and at the end-reperfusion, tissue was harvested for mitochondrial isolation and transmission electron microscopy (TEM). Myocardial and mitochondrial ultrastructure was examined. Furthermore, Rate of reactive oxygen species (ROS) generating were determined at different times.

Results 1. When 30-min reperfusion compared with 20-minute equilibration, significant differences were found in LVDP,LVEDP,DP,HR and CF(P<0.01)as well as TEM，showing that myocardial and mitochondrial ultrastructure were damaged remarkably；

2. When group H compared with group D and group 5HD+H、C, significant differences were found in LVDP, LVEDP, DP, HR and CF(P<0.01)as well as TEM shew that myocardial and mitochondrial ultrastructure was improved remarkably.

3. When group H compared with group D、C and 5HD+H, there were significant differences in rate of ROS generating(P<0.01).

Conclusions Hyperpolarized cardioplegia with mitoKATP opened in the early time of myocardial ischemia is superior to improve myocardial performance, myocardial and mitochondrial ultrastructure, rate of ROS generation. And, it shows that mitochondrial preservation is one of mechanisms of myocardial protection.