Effects of non-invasive limb ischemic preconditioning on endothelial function after myocardial ischemia-reperfusion injury
10.3969/j.issn.1001-1978.2014.12.015
- VernacularTitle:无创肢体缺血预适应对心肌缺血／再灌注损伤内皮功能的影响
- Author:
Weijia CHEN
;
Dongming LIU
;
Zhaoyan QIANG
;
Ke WEN
;
Hengjie YUAN
;
Yi KANG
;
Jianshi LOU
;
Yanna WU
- Publication Type:Journal Article
- Keywords:
limb ischemic preconditioning;
myocardi-al ischemia-reperfusion;
ATP-sensitive potassium channel;
nitric oxide;
endothelin-1;
mir-30a-3p
- From:
Chinese Pharmacological Bulletin
2014;(12):1692-1697
- CountryChina
- Language:Chinese
-
Abstract:
Aims To investigate the protective effects of noninvasive limb ischemic preconditioning (LIPC) on myocardial ischemia-reperfusion (I /R)injury,and to explore the mechanism.Methods Healthy male Wistar rats were divided randomly into I /R,I /R +LIPC,I /R +5-Hydroxydecanoate (5-HD)and I /R +LIPC +5-HD groups.The I /R +LIPC and I /R +LIPC-5-HD groups of rats were subjected to three cy-cles of LIPC induction per day with 5 min of reperfu-sion after occlusion for 5 min at the left hind limb for 3 days.All rats were subjected to myocardial I /R injury on the fourth day.The I /R +5-HD and I /R +LIPC-5-HD groups of rats were given the inhibitor of ATP-sen-sitive potassium channel 5-HD before and during myo-cardial I /R injury. Results Compared with I /R group,LIPC reduced myocardial infarct size (P <0.05),lowered cardiocyte apoptosis index and Fas, FasL positive cell number (P <0.01 ),increased the reduced nitric oxide (NO)/endothelin (ET)-1 ratio (P <0.05)in serum in I /R +LIPC group.5-HD a-bolished the protective effects induced by LIPC in I /R+LIPC-5-HD group.Compared with normal myocardi-al tissue,expression of mir-30a-3p was increased in I /R group (P <0.01 )and was decreased in LIPC group (P <0.01 ).Conclusion LIPC alleviates myocardial I /R injury and improves endothelial function. The mechanism may be related with the opening of ATP-sensitive potassium channel,regulating the balance be-tween NO and ET-1 and decreasing the expression of myocardial mir-30a-3p.
