Reference : Effect of serotonergic blockade on calf pulmonary function after the intravenous admi...
Scientific journals : Article
Life sciences : Veterinary medicine & animal health
http://hdl.handle.net/2268/6748
Effect of serotonergic blockade on calf pulmonary function after the intravenous administration of 3-methylindole
English
Linden, Annick mailto [Université de Liège - ULiège > Département des maladies infectieuses et parasitaires > > >]
Desmecht, Daniel mailto [Université de Liège - ULiège > Département de morphologie et pathologie > Pathologie spéciale et autopsies >]
Vandenput, Sandrina mailto [Université de Liège - ULiège > CARE "Le Réseau des bibliothèques" > Bibliothèque des Sciences de la vie >]
Van de Weerdt, Marie-Lys [> > > >]
Lekeux, Pierre mailto [Université de Liège - ULiège > Département de sciences fonctionnelles > Physiologie >]
1996
Journal of Comparative Pathology
Academic Press
114
4
361-371
Yes (verified by ORBi)
International
0021-9975
Liverpool
United Kingdom
[en] This study was designed to investigate whether 3-methylindole (3-Mi), a tryptamine analogue, could cause pulmonary injury in calves other than by cytotoxicity. Injection of 3-Mi resulted in a marked increase of respiratory rate, decrease of tidal volume and increase in minute ventilation. Pulmonary mechanics values were also profoundly affected, lung dynamic compliance being reduced to approximately one-third of its baseline value and total pulmonary resistance being increased two-fold. Arterial oxygen partial pressure was dramatically reduced. Successive challenges with 3-Mi after physiological saline pretreatment resulted in quantitatively identical alterations of pulmonary function values. Conversely, all these ventilatory, mechanical and gas exchange changes were abolished by pretreatment with serotonergic antagonists. It was concluded that intravenous administration of 3-Mi to healthy calves induced immediate and reversible bronchoconstriction which affected both central and peripheral airways. Because the effect was abolished by pretreatment with antiserotonin drugs, it is suggested that 3-Mi acts either directly by stimulating serotonergic receptors or indirectly through the release of serotonin from platelets. Current concepts of the physiopathological cascade underlying the toxicity of 3-Mi should, therefore, be re-evaluated in the light of this pharmacological mechanism.
Researchers ; Professionals ; Students
http://hdl.handle.net/2268/6748
10.1016/S0021-9975(96)80012-0

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