BAROREFLEX DYSFUNCTION IN DIABETES-MELLITUS .1. SELECTIVE IMPAIRMENT OF PARASYMPATHETIC CONTROL OF HEART-RATE

Citation
Ts. Mcdowell et al., BAROREFLEX DYSFUNCTION IN DIABETES-MELLITUS .1. SELECTIVE IMPAIRMENT OF PARASYMPATHETIC CONTROL OF HEART-RATE, The American journal of physiology, 266(1), 1994, pp. 80000235-80000243
Citations number
30
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
266
Issue
1
Year of publication
1994
Part
2
Pages
80000235 - 80000243
Database
ISI
SICI code
0002-9513(1994)266:1<80000235:BDID.S>2.0.ZU;2-1
Abstract
The purpose of this study was to determine the effect of diabetes mell itus on baroreflex control of heart rate. Diabetes (blood glucose = 37 8 +/- 21 mg/dl) was induced in rabbits by alloxan (n = 9). Alloxantrea ted rabbits that remained normoglycemic (n = 9) and rabbits given sali ne instead of alloxan (n = 5) served as controls. Baroreflex control o f heart rate was evaluated in conscious rabbits by measuring changes i n 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 pressu re decreased significantly from -1.8 +/- 0.3 beats.min-1.mmHg-1 before alloxan (n = 9) to -0.9 +/- 0.1 and -0.9 +/- 0.3 beats.min-1.mmHg-1 a fter 12 and 24 wk of diabetes, respectively (n = 8; P < 0.05). There w as no significant change in baroreflex gain in either alloxan-treated or saline-treated normoglycemic rabbits. Baroreflex-mediated bradycard ia was not influenced significantly after P-adrenergic blockade with p ropranolol (1 mg/kg) and was still impaired in diabetic vs. control ra bbits after propranolol. The gain of the baroreflex-mediated tachycard ia in response to decreased pressure was not altered in any of the thr ee groups. Propranolol significantly decreased but did not abolish bar oreflex-mediated tachycardia. Neither the vagal nor the sympathetic co mponent of the tachycardia was altered significantly by diabetes. We c onclude that in diabetic rabbits 1) baroreflex-mediated bradycardia is impaired, whereas reflex tachycardia is preserved; 2) the impairment of baroreflex-mediated bradycardia is caused by a defect in parasympat hetic control; and 3) the preservation of baroreflex-mediated tachycar dia reflects preservation of both sympathetic activation and parasympa thetic withdrawal. We speculate that selective impairment of parasympa thetic activation may contribute to the increased incidence of arrhyth mias and sudden death in diabetes.