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

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.