In six spontaneously breathing pigs, we studied the role of arachidonic acid metabolites, endothelin-1 (ET-1) and K+ATP channels on systemic and pulmonary vascular beds, during hypoxia (O2 10% in air). The effects of hypoxia were studied in control conditions, after block of prostanoids by indomethacin, after block of ET-1 receptors by Bosentan and after opening of K+ATP channels by Cromakalim. Bosentan and Cromakalim were administered after pretreatment with indomethacin. Results show that the pulmonary hypertension and the modest increase in systemic arterial pressure hypoxia-dependent are caused by the release of ET-1 and can be counterbalanced by the opening of K+ATP channels. Hypoxia does not modify cardiac output and heart rate, therefore the observed changes in pulmonary and systemic vascular resistances seem essentialy due to a change in pulmonary and systemic pressures.

Ruolo dell’endotelina-1 (ET-1) e dei canali K+ATP sulla circolazione polmonare e sistemica nel suino in condizioni di ipossia / M.G. Clement, M. Albertini. - In: ATTI DELLA SOCIETA' ITALIANA DELLE SCIENZE VETERINARIE. - ISSN 1721-1980. - 51:(1997), pp. 469-470. ((Intervento presentato al 51. convegno LI Congresso SISVet tenutosi a Bologna nel 1997.

Ruolo dell’endotelina-1 (ET-1) e dei canali K+ATP sulla circolazione polmonare e sistemica nel suino in condizioni di ipossia

M.G. Clement
Primo
;
M. Albertini
Ultimo
1997

Abstract

In six spontaneously breathing pigs, we studied the role of arachidonic acid metabolites, endothelin-1 (ET-1) and K+ATP channels on systemic and pulmonary vascular beds, during hypoxia (O2 10% in air). The effects of hypoxia were studied in control conditions, after block of prostanoids by indomethacin, after block of ET-1 receptors by Bosentan and after opening of K+ATP channels by Cromakalim. Bosentan and Cromakalim were administered after pretreatment with indomethacin. Results show that the pulmonary hypertension and the modest increase in systemic arterial pressure hypoxia-dependent are caused by the release of ET-1 and can be counterbalanced by the opening of K+ATP channels. Hypoxia does not modify cardiac output and heart rate, therefore the observed changes in pulmonary and systemic vascular resistances seem essentialy due to a change in pulmonary and systemic pressures.
pig ; cardiovascular system ; physiology ; hypoxia ; K+ATP ; ET-1
Settore VET/02 - Fisiologia Veterinaria
1997
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/185403
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