摘要
目的:探讨线粒体钙单向转运体是否参予远距预处理的心肌保护作用。方法:采用在体结扎冠状动脉左前降支30 min和复灌120 min复制局部心肌缺血/复灌损伤模型,采用动脉夹夹闭右下肢股动脉5 min,松开复灌5 min,共3个循环,行大鼠肢体远距预处理。结果:与单纯缺血/复灌组相比,静脉注射线粒体钙单向转运体抑制剂钌红或肢体远距预处理明显降低心脏缺血/复灌后的梗死面积(钌红组心肌梗死面积26.34%±5.4%,远距预处理组20.38%±2.50%,与单纯缺血复灌组50.96%±5.96%相比,P<0.01)和复灌10 min血浆冠脉流出液中LDH活性[钌红组LDH活性(280.74±28.42)U/L,远距预处理组(270.5±8.91)U/L,与单纯缺血复灌组(338.75±38.60)U/ L相比,P<0.01];线粒体钙单向转运体激动剂精胺可减弱远距预处理降低心肌梗死面积(精胺+远距预处理组心肌梗死面积40.77%±9.20%与远距预处理组20.38%±2.50%相比,P<0.01)和LDH活性[精胺+远距预处理组LDH活性(382.74±43.08)U/L,与远距预处理组LDH活性(270.50±8.91)U/L相比,P<0.01]的作用。结论:肢体远距预处理诱导的抗心肌缺血/复灌损伤的保护作用可能与线粒体钙单向转运体的抑制有关。
Ahn: To investigate whether mitochondrial calcium uniporter participates in the cardioprotection of remote preconditioning in rat hearts subjected to ischemia and repeffusion in vivo. Methods: Rat hearts were subjected to 30 rain regioal ischemia(occlusion of left anterior descending artery) and 120 min reperfusion in vivo. Remote preconditioning was induced by three cycles of 5 min of right femoral artery occlusion followed by 5 min of reperfusion. The mean arterial blood pressure, heart rate, infarct size, and lactate dehydrogenase(LDH) activity in plasma during reperfusion were measured. Results: Remote preconditioning reduced both the infarct size and LDH release during reperfusion. Ruthenium red, an inhibitor of mitochondrial calcium uniporter, also decreased both the infarct size and LDH release. Administration of spermine, an activator of mitochondrial calcium tmiporter, canceled the reduction of infarct size and LDH release induced by remote preconditioning. Conclusion: These results indicate that remote preconditioning protects myocardimn against ischemia and reperfusion injury, that effect may be related to inhibiting mitochondrial calcium uniporter opening.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2009年第1期50-54,共5页
Chinese Journal of Applied Physiology
基金
浙江省科技厅基金资助(2006C33070)
关键词
远距预处理
心肌
缺血/复灌
线粒体钙单向转运体
remote preconditioning
heart
ischemia/reperfusion
mitochondrial calcium uniperter