title: Contribution of vasopressor and plasma kininogen changes towards acute adrenaline pulmonary edema in the rat.
abstract: Acute pulmonary edema, evidenced by increased lung/body weight ratios, was evoked in rats within 5 min following the intravenous injection of 16-40 mug/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 trysin 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 mug/kg of carbamylcholine administered together with 40 mug/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.
mesh_terms: D000818:Animals; D007611:Aprotinin / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D002199:Capillary Permeability; D002217:Carbachol / Q000494:pharmacology; D004837:Epinephrine; D007704:Kininogens / Q000097:blood*; D008297:Male; D011654:Pulmonary Edema / Q000097:blood* / Q000139:chemically induced / Q000503:physiopathology; D051381:Rats; D013025:Glycine max; D014361:Trypsin Inhibitors / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D007704:Kininogens; D014361:Trypsin Inhibitors; D002217:Carbachol; D007611:Aprotinin; D001241:Aspirin; D004837:Epinephrine