Ischemic postconditioning attenuates myocardial cell injury by ischemia-reperfusion injury in rabbits
- VernacularTitle:缺血后处理减轻兔缺血再灌注心肌细胞损伤
- Author:
Yan HE
;
Zhiyu ZENG
;
Jinyi LI
;
Guoqiang ZHONG
;
Wei LI
;
Weike LI
;
Honghong KE
- Publication Type:Journal Article
- Keywords:
isehemia reperfusion;
postconditioning;
mitochondria;
apoptosis
- From:
Basic & Clinical Medicine
2010;30(2):133-138
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of ischemic postconditioning on apoptosis, structural and functional changes of mitochondria induced by myocardial isehemia/reperfusion (I/R) injury of rabbits and potential mechanism. Methods Eighty healthy rabbits were divided randomly into five groups: sham operation group ( Group Sham) , ischemic reperfusion group (Group IR) , ischemic preconditioning group (Group IP) , ischemic postconditioning group (Group PC) and 5-HD plus ischemic postconditioning group (Group PC +5-HD). All rabbits in the five groups were killed 4 h after reperfusion. The hearts were quickly collected for microscopy by TUNEL. We observed ultrastructural changes of myocardium under electron microscope and examined mitochondrial membrane potential and Ca~(2+) concentration, MDA content and SOD activity of myocardial mitochondria. Results Compared with group IR, the damage of mitoehondrial ultrastrueture was milder, the apoptosis rate decreased and Ca concentration and MDA content were much lower in group IP and group PC ( P < 0. 05 ). Mitochondrial membrane potential and SOD activity of myocardial mitochondria in group IP and group PC was significantly higher than that in group IR(P<0.05). The protective effect of PC against I/R injury was partially counteracted by 5-HD .Conclusion Ischemic posteonditioning can protect the heart from I/R injury, this is supported by improvement mitochondrial ultrastructure and by decreasing apoptosis, increasing mitochondrial membrane potential and SOD activity, alleviating Ca~(2+) overload and decreasing MDA content in myocardial mitochondria. The cardio protective effects may be explained by mitochondrial ATP sensitive potassium channel.
