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冠状动脉闭塞和再灌注期间局部心肌间质去甲肾上腺素动力学

Regional myocardial interstitial norepinephrine kinetics during coronary occlusion and reperfusion.

作者信息

Shindo T, Akiyama T, Yamazaki T, Ninomiya I

机构信息

Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Osaka, Japan.

出版信息

Am J Physiol. 1996 Jan;270(1 Pt 2):H245-51. doi: 10.1152/ajpheart.1996.270.1.H245.

Abstract

We investigated myocardial interstitial norepinephrine kinetics in both the ischemic and nonischemic regions during reperfusion after 40 min of coronary occlusion in anesthetized cats. By use of a cardiac dialysis technique, dialysate norepinephrine contents from both regions were monitored as an index of myocardial interstitial norepinephrine levels. For vehicle perfusate (n = 8), the accumulated dialysate norepinephrine level in the postischemic region decreased from 3,010 +/- 923 pg/ml at 30-40 min of occlusion to 957 +/- 178 pg/ml at 0-10 min of reperfusion and returned to near control level at 30-40 min of reperfusion. After 40 min of reperfusion, there were no significant differences in tyramine (100 micrograms/ml, norepinephrine-releasing sympathomimetic amine)-induced norepinephrine release between both regions. For perfusate containing 100 microM desipramine (neural uptake inhibitor, n = 6), at 0-10 min of reperfusion, the dialysate norepinephrine in the postischemic region did not significantly decrease. The dialysate norepinephrine then returned to near preocclusion level at 30-40 min of reperfusion. These data suggest that reperfusion rapidly returns accumulated myocardial norepinephrine to the preischemic level and neuronal norepinephrine uptake greatly contributes to this return in the early phase of reperfusion. Forty minutes of coronary occlusion cause neither norepinephrine exhaustion nor irreversible impairment of norepinephrine uptake function in nerve terminals.

摘要

我们研究了麻醉猫冠状动脉闭塞40分钟后再灌注期间缺血和非缺血区域心肌间质去甲肾上腺素的动力学。通过使用心脏透析技术,监测两个区域透析液中去甲肾上腺素的含量,作为心肌间质去甲肾上腺素水平的指标。对于载体灌注液(n = 8),缺血后区域透析液中去甲肾上腺素的累积水平在闭塞30 - 40分钟时从3,010±923 pg/ml降至再灌注0 - 10分钟时的957±178 pg/ml,并在再灌注30 - 40分钟时恢复到接近对照水平。再灌注40分钟后,两个区域之间在酪胺(100微克/毫升,去甲肾上腺素释放拟交感胺)诱导的去甲肾上腺素释放方面没有显著差异。对于含有100微摩尔地昔帕明(神经摄取抑制剂,n = 6)的灌注液,在再灌注0 - 10分钟时,缺血后区域透析液中的去甲肾上腺素没有显著下降。然后在再灌注30 - 40分钟时,透析液中的去甲肾上腺素恢复到接近闭塞前的水平。这些数据表明,再灌注迅速将累积的心肌去甲肾上腺素恢复到缺血前水平,并且神经元去甲肾上腺素摄取在再灌注早期对这种恢复有很大贡献。冠状动脉闭塞40分钟既不会导致去甲肾上腺素耗竭,也不会导致神经末梢去甲肾上腺素摄取功能的不可逆损害。

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