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AJP - Heart and Circulatory Physiology, Vol 256, Issue 5 1322-H1327, Copyright © 1989 by American Physiological Society
ARTICLES |
T. Matsuki, M. V. Cohen, G. Holt, J. Ayling, D. J. Hearse and J. M. Downey
Department of Physiology, College of Medicine, University of South Alabama, Mobile 36688.
We determined whether chronic chemical sympathetic denervation could protect the rabbit heart against ischemia. Rabbits received 10 mg/kg 6-hydroxydopamine (6-HD) twice during the first week, then 100 mg.kg-1.wk-1 for the following 7 wk. After this interval the rabbits were anesthetized, the chests were opened, and in each a coronary branch was occluded for 45 min followed by reperfusion for 3 h. Collateral flow was determined with radioactive microspheres during coronary occlusion. Flow to the ischemic myocardium of the 6-HD group (0.06 +/- 0.03 ml.min-1.g-1) was not significantly different from that in the control group (0.04 +/- 0.02 ml.min-1.g-1). Infarct size was determined with triphenyltetrazolium chloride staining. Average infarct size calculated as a percentage of risk zone was similar in the 6-HD and control groups (59 +/- 15 and 60 +/- 12%, respectively). We conclude that chronic chemical sympathectomy does not induce collateral growth in the rabbit heart. Furthermore, endogenous catecholamines do not contribute to injury in the ischemic rabbit heart.
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