Decreased vulnerability to ventricular fibrillation by vasodilator-induced baroreceptor sensitisation.
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 micrograms X kg-1 X min-1) caused a fall in ventricular fibrillation threshold from 30 to 20 mA (P less than 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.
D000527:Alprostadil; D000818:Animals; D003714:Denervation; D004285:Dogs; D011464:Epoprostenol / Q000494:pharmacology; D005260:Female; D008297:Male; D005996:Nitroglycerin / Q000494:pharmacology; D009638:Norepinephrine / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D011311:Pressoreceptors / Q000187:drug effects* / Q000503:physiopathology; D011458:Prostaglandins E / Q000494:pharmacology; D014693:Ventricular Fibrillation / Q000139:chemically induced / Q000503:physiopathology*
D011458:Prostaglandins E; D011464:Epoprostenol; D000527:Alprostadil; D005996:Nitroglycerin; D009638:Norepinephrine