Reference : Interactions between acetylcholine and substance P effects on lung mechanics in the r...
Scientific journals : Article
Life sciences : Veterinary medicine & animal health
Human health sciences : Pharmacy, pharmacology & toxicology
Interactions between acetylcholine and substance P effects on lung mechanics in the rabbit.
Delaunois, Annie mailto [Université de Liège - ULg > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Gustin, Pascal mailto [Université de Liège - ULg > Département de sciences fonctionnelles > Pharmacologie, pharmacothérapie et toxicologie >]
Segura, P. [> > > >]
Vargas, M. [> > > >]
Ansay, Michel mailto [Université de Liège - ULg > Services généraux (Faculté de médecine vétérinaire) > Relations académiques et scientifiques (Méd. vétérinaire) >]
Fundamental & Clinical Pharmacology
Blackwell Science
Yes (verified by ORBi)
United Kingdom
[en] Acetylcholine/pharmacology ; Analysis of Variance ; Animals ; Benzamides/pharmacology ; Dose-Response Relationship, Drug ; Female ; Histamine/pharmacology ; Lung/blood supply/drug effects ; Male ; Muscle, Smooth/drug effects ; Perfusion ; Piperidines/pharmacology ; Pulmonary Circulation/drug effects ; Pulmonary Edema/chemically induced ; Quinuclidines/pharmacology ; Rabbits ; Substance P/antagonists & inhibitors/pharmacology ; Vasoconstriction/drug effects
[en] The pharmacological mechanisms involved in the acetylcholine (ACh)- and substance P (SP)-induced changes in pulmonary mechanics were studied in isolated perfused rabbit lungs. Tracheal pressure (Ptr) and airflow were measured by a Fleisch pneumotachograph and pressure transducers. Air volume, lung resistance (RL) and dynamic compliance (Cdyn) were calculated. ACh induced a dose-dependent increase in Ptr and RL, and a decrease in Cdyn. These effects were strongly prevented by atropine, and partly by SR140333, a neurokinin NK1 receptor antagonist; SR48968, a neurokinin NK2 receptor antagonist; indomethacin and antihistaminics. Ketanserin had no significant protective effect against ACh. SP also induced concentration-dependent increases in RL and decreases in Cdyn. SR140333 and atropine strongly inhibited the effects of SP, while ketanserin, SR48968, antihistaminics and indomethacin did not protect the lungs against this drug. 5-hydroxytryptamine induced no significant change in lung mechanic parameters. Cumulative concentrations of histamine increased RL and decreased Cdyn. We conclude that ACh-induced changes in lung resistance and compliance are in part mediated by a direct effect on airway smooth muscle and in part by the stimulation of C fibers, by the release of histamine from mast cells and by the synthesis of arachidonic acid metabolites. In turn, the effects of SP on lung mechanics are partly due to cholinergic activation.
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