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AJP - Heart and Circulatory Physiology, Vol 266, Issue 1 235-H243, Copyright © 1994 by American Physiological Society
ARTICLES |
T. S. McDowell, M. W. Chapleau, G. Hajduczok and F. M. Abboud
Cardiovascular Center, University of Iowa, Iowa City.
The purpose of this study was to determine the effect of diabetes mellitus on baroreflex control of heart rate. Diabetes (blood glucose = 378 +/- 21 mg/dl) was induced in rabbits by alloxan (n = 9). Alloxan-treated rabbits that remained normoglycemic (n = 9) and rabbits given saline instead of alloxan (n = 5) served as controls. Baroreflex control of heart rate was evaluated in conscious rabbits by measuring changes in heart rate during phenylephrine-induced increases and nitroglycerin-induced decreases in arterial pressure. In diabetic rabbits, the gain of the baroreflex-mediated bradycardia in response to increased pressure decreased significantly from -1.8 +/- 0.3 beats.min-1 x mmHg-1 before alloxan (n = 9) to -0.9 +/- 0.1 and -0.9 +/- 0.3 beats.min-1 x mmHg-1 after 12 and 24 wk of diabetes, respectively (n = 8; P < 0.05). There was no significant change in baroreflex gain in either alloxan-treated or saline-treated normoglycemic rabbits. Baroreflex-mediated bradycardia was not influenced significantly after beta-adrenergic blockade with propranolol (1 mg/kg) and was still impaired in diabetic vs. control rabbits after propranolol. The gain of the baroreflex-mediated tachycardia in response to decreased pressure was not altered in any of the three groups. Propranolol significantly decreased but did not abolish baroreflex-mediated tachycardia. Neither the vagal nor the sympathetic component of the tachycardia was altered significantly by diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)
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