Reference : Role of Neuropeptides in Acetylcholine-Induced Edema in Isolated and Perfused Rabbit Lungs
Scientific journals : Article
Life sciences : Veterinary medicine & animal health
Role of Neuropeptides in Acetylcholine-Induced Edema in Isolated and Perfused Rabbit Lungs
Delaunois, Annie [Université de Liège - ULiège > > > >]
Gustin, Pascal mailto [Université de Liège - ULiège > Département de sciences fonctionnelles > Pharmacologie, pharmacothérapie et toxicologie >]
Ansay, Michel [Université de Liège - ULiège > Faculté de médecine vétérinaire > > >]
Journal of Pharmacology and Experimental Therapeutics (The)
American Society for Pharmacology and Experimental Therapeutics
Yes (verified by ORBi)
[en] Acetyilcholine ; Edema ; Rabbit
[en] Changes in pulmonary endothelial permeability and in microvascular hemodynamics in response to cumulative concentrations of acetylcholine (ACh) (10(-8) M to 10(-5) M) were investigated in isolated, perfused rabbit lungs. The total pressure gradient was partitioned into four components: arterial, pre- and postcapillary and venous. The capillary filtration coefficient (Kf, c) also was evaluated. ACh caused a significant increase in arterial and precapillary pressures at concentrations higher than 3 x 10(-6) M. The total pressure gradient and precapillary were significantly increased whereas arterial, postcapillary and venous pressure gradient remained unchanged. In papaverine (3 x 10(-4) M)-pretreated lungs, the vasoconstriction was abolished and a concentration-dependent increase in Kf,c was recorded from 10(-8) to 10(-5) M ACh. This reaction was accompanied by pulmonary edema. Atropine, indomethacin, aspirin, ketanserin, clonidine, morphine and (+/-)-CP 96-345, an antagonist of neurokinin NK1 receptors, completely prevented the effects of ACh on Kf,c. In contrast, cromolyn sodium and SR48968, a neurokinin NK2 antagonist, did not inhibit the response to ACh. Terfenadine together with cimetidine had a partially inhibitory effect. Changes in the Kf, c similar to those observed with ACh were induced by capsaicin (10(-4) M) by exogenous substance P (10(-7) M) and by 5-hydroxytryptamine (5-HT) (10(-4) M). The effects of SP were inhibited by aspirin, (+/-)-CP 96,345 and ketanserin, but not by atropine and antihistaminics. 5-HT effects were prevented by aspirin and not by (+/-)-CP 96,345. It was concluded that ACh-induced pulmonary edema was due to an increase in the capillary filtration coefficient.(ABSTRACT TRUNCATED AT 250 WORDS)
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