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. ClementPrimo
;M. AlbertiniUltimo
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.Pubblicazioni consigliate
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