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Cardiovascular Research 1983 17(2):106-112; doi:10.1093/cvr/17.2.106
© 1983 by European Society of Cardiology
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Copyright © 1983, European Society of Cardiology

Decreased vulnerability to ventricular fibrillation by vasodilator-induced baroreceptor sensitisation

PETER R KOWEY*, RICHARD L VERRIER and BERNARD LOWN

From the Cardiovascular Laboratories, Department of Nutrition, Harvard School of Public Health and the Cardiovascular Division, Department of Medicine of the Brigham and Women's Hospital, Harvard Medical School, Boston, MA

* Send reprint requests to: Peter R Kowey, MD, Cardiology Division, The Medical College of Pennsylvania, 3300 Henry Avenue, Philadelphia, Pennsylvania 19129, USA.

Vulnerability to ventricular fibrillation (VF) is affected by changes in systemic arterial blood pressure which are mediated through the sympathetic nervous system. We determined that small doses of a vasodilator drug can abolish the enhanced ventricular vulnerability induced by norepinephrine infusion. Noradrenaline (0.5 µg·kg–l·min–1) caused a fall in ventricular fibrillation threshold from 30 to 20 mA (P<0.001). Pretreatment with prostaglandin E1, I2 or nitroglycerin at doses which reduced mean arterial blood pressure by 0.7 to 1.3 kPa (5 to 10 mmHg) abolished the enhanced vulnerability produced by noradrenaline. Following baroreceptor denervation, these agents no longer afforded protection against the profibrillatory action of noradrenaline. We conclude that small doses of vasodilator agents can augment ventricular electrical stability. The mechanism for this protective action appears to be a decrease in cardiac sympathetic tone resulting from vasodilatation of baroreceptor areas.

Dr Kowey is the recipient of a National Research Service Award from the National Institutes of Health, Bethesda, MD.


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