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U 50 488H预处理大鼠诱导的延迟性心脏保护效应及其机制(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2003年第5期
页码:
397-399
栏目:
实验研究
出版日期:
2003-09-01

文章信息/Info

Title:
The delayed cardioprotection with U50 488H pretreatment in rat heart and underlying mechanism
作者:
陈迈1; 贾国良1; 裴建明2; 周京军2
第四军医大学: 1. 西京医院心脏内科, 2. 生理学教研室, 陕西 西安710032
Author(s):
CHEN Mai1;  JIA Gou-liang1;  PEI Jian-ming2;  ZHOU Jing-jun2
1.Department of Cardiology, Xijing Hospital,2.Department of Physiology, Fourth Military Medical University, Xian, Shaanxi 710032, China
关键词:
U 50 488H; 心脏梗死面积; 心肌细胞; Ca2+
Keywords:
U 50 488H;  infarct size;  cardiomyocyte;  intracellular Ca2+
分类号:
Q463　
DOI:
-
文献标识码:
A
摘要:
目的:trans-(±)-3, 4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl) cyclohexyl]-benzeneacetamide (U 50 488H) 是J阿片受体的选择性激动剂。实验观察静脉注射U 50 488H (10mg?k g) 24h后对心脏的延迟性保护作用及其细胞内机制。方法:①采用离体灌流的大鼠心脏模型, 通过局部缺血?再灌注, 以心脏梗死面积作为心脏损伤的判定标准, 观察U 50 488H 预处理(UP) 对心脏的延迟性保护作用。②采用分离的大鼠心肌细胞模型, 通过代谢抑制 (metabolic inhibition, M I) ,观察U P对心肌细胞内静息Ca2+ 和电诱导Ca2+ 瞬变的影响。结果: ①U P 可显著降低心脏梗死面积; ②U P 的大鼠心肌细胞在MI 时, 心肌细胞内静息Ca2+ 的升高程度较对照组显著降低; ③U P 的大鼠心肌细胞在M I 时, 心肌细胞电诱导Ca2+ 瞬变的降低程度较对照组显著减少。上述作用均可被U P 前10 min 腹腔注射J阿片受体的选择性阻断剂nor-binaltorphimine(10 mg?kg) 阻断。结论: U 50 488H 可通过刺激J阿片受体产生延迟性的心脏保护作用, 此作用与心肌细胞内的Ca2+ 稳态的调节有关。
Abstract:
AIM: To determine whether U 50 488H, a selective agonist of J opioid receptor, induces delayed cardioprotection in perfused rat heart and underlying cellular mechanism. METHODS: U 50 488H in 10 mg?kg was given in travenously to the rat. 24 h later, the rat was killed and the isolated heart was subjected to ischemia? reperfusion. Myocardial injury was determined by measuring the infarct size at the end of the reperfusion. In addition, the ventricular myocytes were isolated, and the resting in tracellular Ca2+ ([Ca2+ ]i) and the electrically-induced [Ca2+]i transient were also observed upon the metabolic inhibition. RESULTS: U 50 488H pretreatment (UP) significantly reduced the infarct size, at tenuated the elevation in resting [Ca2+]i and reduction in electrically-induced [Ca2+]i in cardiomyocytes subjected to metabolic inhibition. The effects of UP were abolished w hen the selective J opioid receptor an tagonist nor-binaltorphimine at 10mg?kg was administered 10m in prior to the U 50 488H administration. CONCLUSION: The results demonstrate that UP induces the delayed cardioprotection by stimulating cardiac J opioid receptor, and that the prevention or at tenuation of alterations in Ca2+ homeostasis induced by ischemic insult is involved in the cardioprotective effect of UP.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2002-12-30.
更新日期/Last Update: 2003-09-01