In 10 anaesthetized and mechanically ventilate Large White pigs we analysed the activity of Endothelin-1 (ET-1) and the involvement of prostacyclin (PGI2) and nitric oxide (NO) as modulators of ET-1 activity. Parameters evaluated were: systemic (MAP) and pulmonary arterial pressure (MPAP), heart rate (HR), cardiac output (CO) and systemic (SVR) and pulmonary vascular resistances (PVR). Results showed that ET-1 (100 pmol/kg i.v.) induces a biphasic response both on pulmonary and systemic vascular bed. This was characterised by an early and transient hypotension, followed by an hypertensive activity lasting about 20'. Blocking NO by NG-nitro-L-arginine methyl ester (L-NAME 5 mg/kg i.v.), or PGI2 by indomethacin (3 mg/kg i.v.), the hypotensive activity ET-1-dependent on systemic vascular bed, at difference to pulmonary one, disappears. This data show that ET-1 at systemic level induces the release of NO and PGI2, while at pulmonary level its hypotensive activity is probably due to other vasoactive metabolites.
I vasodilatatori endoteliali controbilanciano l’azione dell’endotelina-1 / M. Albertini. - In: ATTI DELLA SOCIETA' ITALIANA DELLE SCIENZE VETERINARIE. - ISSN 1721-1980. - 49:(1995), pp. 251-252. ((Intervento presentato al 49. convegno XLIX Convegno SISVet tenutosi a Salsomaggiore Terme nel 1995.
I vasodilatatori endoteliali controbilanciano l’azione dell’endotelina-1
M. AlbertiniPrimo
1995
Abstract
In 10 anaesthetized and mechanically ventilate Large White pigs we analysed the activity of Endothelin-1 (ET-1) and the involvement of prostacyclin (PGI2) and nitric oxide (NO) as modulators of ET-1 activity. Parameters evaluated were: systemic (MAP) and pulmonary arterial pressure (MPAP), heart rate (HR), cardiac output (CO) and systemic (SVR) and pulmonary vascular resistances (PVR). Results showed that ET-1 (100 pmol/kg i.v.) induces a biphasic response both on pulmonary and systemic vascular bed. This was characterised by an early and transient hypotension, followed by an hypertensive activity lasting about 20'. Blocking NO by NG-nitro-L-arginine methyl ester (L-NAME 5 mg/kg i.v.), or PGI2 by indomethacin (3 mg/kg i.v.), the hypotensive activity ET-1-dependent on systemic vascular bed, at difference to pulmonary one, disappears. This data show that ET-1 at systemic level induces the release of NO and PGI2, while at pulmonary level its hypotensive activity is probably due to other vasoactive metabolites.Pubblicazioni consigliate
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