Contribution of vasopressor and plasma kininogen changes towards acute adrenaline pulmonary edema in the rat

Summary

Acute pulmonary edema, evidenced by increased lung/body weight ratios, was evoked in rats within 5 min following the intravenous injection of 16–40 μg/kg of adrenaline. This change was accompanied by a decrease of 40% of circulatory kininogen not due to generalized plasma protein loss. Rats treated 10–20 min prior to adrenaline with 10 mg/kg of acetylsalicylate (Aspirin^®), 1000 KIU/kg of Kunitz anti-protease (Trasylol^®), or 10 mg/kg of soybean trypsin inhibitor (SBTI), failed to exhibit pulmonary edema or decreased plasma kininogen levels, but were as sensitive as untreated animals to the arterial hypertensive effect of adrenaline. 4.8 μg/kg of carbamylcholine administered together with 40 μg/kg of adrenaline, prevented pulmonary edema. Carbamylcholine did not reduce plasma kininogen consumption by adrenaline, but effectively decreased the raised systolic arterial blood pressure, the increased systolic-diastolic pressure interval as well as the reflex slowing of the heart presented by adrenaline-treated rats. It seems that in the adrenaline-treated rat, pulmonary edema results from the joined action of vasopressor effects leading to hydrostatically forced outflow of vascular fluid, and of kinin release leading to increased peripheral vascular permeability.