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AJP - Heart and Circulatory Physiology, Vol 270, Issue 1 245-H251, Copyright © 1996 by American Physiological Society
ARTICLES |
T. Shindo, T. Akiyama, T. Yamazaki and I. Ninomiya
Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Osaka, Japan.
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.
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