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代谢性抑制预处理中Na+/Ca2+交换体反向转运的激活触发预处理后的心肌保护作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第1期
页码:
23-27
栏目:
基础研究
出版日期:
2006-01-01

文章信息/Info

Title:
Activation of reversemode NCX during metabolic inhibition pretreatment triggers the cardioprotection of preconditionin
作者:
李树壮1臧益民1王波3韦耿泽1胡玉珍1秦向阳2裴建明1周京军1
第四军医大学:1. 基础部生理学教研室,2. 药学系化学教研室,陕西 西安 710032;3. 陕西师范大学生命科学院,陕西 西安 710062
Author(s):
LI Shu-Zhuang1ZANG Yi-Min1WANG Bo3WEI Geng-Ze1 HU Yu-Zhen1 QIN Xiang-Yang2PEI Jian-Ming1 ZHOU Jing-Jun1
1.Department of Physiology, 2.Department of Chemistry, Fourth Military Medical University, Xi′an , Shaanxi 710032, China; 3. College of Life Sciences, Shaanxi Normal University, Xi′an , Shaanxi 710062, China
关键词:
钠/钙交换体代谢性抑制预处理心肌保护心室肌细胞
Keywords:
sodium/calcium exchanger metabolic inhibition preconditioning cardioprotectionventricular myocyte
分类号:
R542.2;Q256
DOI:
-
文献标识码:
A
摘要:
目的 研究大鼠心室肌细胞在代谢性抑制预处理中钠/钙交换体(NCX)反向转运的活性,以及NCX反向转运抑制剂是否可以阻止代谢性抑制预处理后的心肌保护作用。方法 酶解法分离制备钙耐受心肌细胞,用Fura2/AM负载,采用双激发荧光光电倍增系统(IonOptix Photometry System)检测钙信号,用单心肌细胞动缘探测技术观察心肌细胞收缩/舒张功能,台盼蓝染色法检测细胞存活率。结果 在代谢性抑制预处理30 min时,NCX反向转运被激活。NCX反向转运抑制剂KBR 7943(0.5 μmol/L)可以抑制代谢性抑制预处理对心肌细胞收缩功能和细胞存活率的作用。NCX激动剂E4031(1 μmol/L)可以模拟代谢性抑制预处理后对心肌细胞收缩功能的保护作用,这一作用也可被KBR 7943阻断。结论 代谢性抑制预处理中,NCX反向转运的激活触发了代谢性抑制预处理后的心肌保护作用;NCX的抑制剂可以阻止代谢性抑制预处理后的心肌保护作用。
Abstract:
AIM To study the activity of reversemode Na+/Ca2+ exchanger (NCX) during metabolic inhibition pretreatment (MIP) of rat ventricular myocytes, and to determine whether the cardioprotection of metabolic inhibition preconditioning can be prevented by reversemode NCX inhibitor. METHODS Single ventricular myocytes were enzymatically isolated and loaded with Fura2/AM. Intracellular calcium concentration ([Ca2+]i) was measured by IonOptix Photometry System. The activity of reversemode NCX was assessed by withdrawal extracellular Na+ and the changes of [Ca2+]i were measured. The amplitude of single myocyte contraction and cell viability were used as indices of cell injury and death, respectively. RESULTS MIP for 30 min significantly increased the activity of reversemode NCX. The effects of MIP on the amplitude of single surviving myocyte contraction and cell viability were attenuated by 0.5 μmol/L KBR 7943(KBR), a specific inhibitor of reversemode NCX, administered before and during MIP. Pretreatment of cells with 1 μmol/L E4031, a selective reversemode NCX enhancer, mimicked the effects of metabolic inhibition preconditioning on cell contraction, which was also blocked by 0.5 μmol/L KBR. CONCLUSION During MIP the activation of reversemode NCX triggers the cardioprotection of metabolic inhibition preconditioning, which can be prevented by blocking NCX reversemode.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期:2005-09-28.Supported by: national natural science foundation of china(No. 30400177) Correspondence to: ZHOU Jingjun, Ph.D.Tel:(029)84774521 Email: jjzhou71@yahoo.com.
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