[非侵入性肢体缺血预处理诱导的心脏保护机制]

[Mechanism of cardioprotection induced by noninvasive limb ischemic preconditioning].

作者信息

Wang Ning-Fu, Xu Jian, Xia Qiang, Gao Qin, Shi Xiao-Xiao, Zhou Zhan-Lin, Wang Lin-Lin, Tong Guo-Xin, Li Hong, Li Pei-Zhang, Zhang Xiong, Ling Feng, Pan Hao, Yang Jian-Min

机构信息

Affiliated Hangzhou Hospital of Nanjing Medical University, Department of Cardiology, First People's Hospital of Hangzhou, Hangzhou 310006, China.

出版信息

Zhonghua Yi Xue Za Zhi. 2009 Jul 28;89(28):1999-2002.

PMID:19950578

Abstract

OBJECTIVE

To verify the inhibitory effect of mitochondrial calcium uniporter in remote preconditioning-induced cardioprotection.

METHODS

By occlusion and reperfusion of left anterior descending artery, the rat hearts were subjected to 30 min regional ischemia and 120 min reperfusion in vivo. Thus the ischemic reperfusion model was established. The rats were randomly assigned to undergo one of the following maneuvers: (1) remote preconditioning; (2) ruthenium red (an inhibitor of mitochondrial calcium uniporter); (3) spermine or SB202190 (an opener of mitochondrial calcium uniporter). Remote preconditioning was elicited by three cycles of 5 min of right femoral artery occlusion interspersed with 5 min of reperfusion. The mean arterial blood pressure, heart rate and lactate dehydrogenase released in plasma were measured during reperfusion but the infarct size was measured after reperfusion.

RESULTS

In comparison with I/R group, remote preconditioning limited infarct size [(20.4 +/- 2.5)% vs (51.0 +/- 6.0)%] and lactate dehydrogenase release [(271 +/- 9) U/L vs (339 +/- 39)U/L] during reperfusion. On the contrary, spermine or SB202190 attenuated the reduction of infarct size and lactate dehydrogenase release induced by remote preconditioning. The group of spermine was [(40.8 +/- 9.2)% vs (20.4 +/- 2.5)%] and [(383 +/- 43) U/L vs (271 +/- 9) U/L] while the group of SB202190 was [(44.3 +/- 6.8)% vs (20.4 +/- 2.5)%] and [(356 +/- 26) U/L vs (271 +/- 9) U/L].

CONCLUSION

Inhibition of mitochondrial calcium uniporter opening is involved in the remote preconditioning-induced cardioprotection.

摘要

目的

验证线粒体钙单向转运体在远程预处理诱导的心脏保护中的抑制作用。

方法

通过结扎和再灌注左前降支动脉，使大鼠心脏在体内经历30分钟的局部缺血和120分钟的再灌注。由此建立缺血再灌注模型。将大鼠随机分为以下操作之一：（1）远程预处理；（2）钌红（线粒体钙单向转运体抑制剂）；（3）精胺或SB202190（线粒体钙单向转运体开放剂）。通过右股动脉闭塞5分钟并穿插5分钟再灌注的三个周期来引发远程预处理。在再灌注期间测量平均动脉血压、心率和血浆中释放的乳酸脱氢酶，但在再灌注后测量梗死面积。

结果

与缺血/再灌注组相比，远程预处理在再灌注期间限制了梗死面积[（20.4±2.5）%对（51.0±6.0）%]和乳酸脱氢酶释放[（271±9）U/L对（339±39）U/L]。相反，精胺或SB202190减弱了远程预处理诱导的梗死面积减小和乳酸脱氢酶释放减少。精胺组为[（40.8±9.2）%对（20.4±2.5）%]和[（383±43）U/L对（271±9）U/L]，而SB202190组为[（44.3±6.8）%对（20.4±2.5）%]和[（356±26）U/L对（271±9）U/L]。