In anaesthetised, paralysed and mechanically ventilated pigs we evaluated the involvement of ET-1 on PAF-dependent respiratory effects, blocking ET A and ETB receptors with BQ123 and BQ788 respectively. To avoid interference by nitric oxide we used L-NAME, an inhibitor of both NO synthases. The results show that PAF causes a decrease in Crs and an increase in Pmax and Pst, evidencing that the change in Rrs is due to a bron-choconstrictor effect and to a change in viscoelastic properties of the respiratory system. PAF did not significantly affect systemic arterial pressure, while caused a marked increase in mean pulmonary arterial pressure (MPAP). The block of ET-1 receptors partially reduced the respiratory effects elicited by PAF, but did not affect the changes in MPAP. In conclusion our results evidence that PAF favours a release of ET-1. This peptide strengthened PAF-dependent bronchoconstriction and impairs viscoelastic properties of the respiratory system.
Involvement of endothelin-1 (ET-1) in PAF-dependent respiratory effects / M. Albertini, S. Mazzola, M.G. Clement. - In: BIOMEDICAL RESEARCH. - ISSN 0970-938X. - 11:3(2000), pp. 239-244.
Involvement of endothelin-1 (ET-1) in PAF-dependent respiratory effects
M. AlbertiniPrimo
;S. MazzolaSecondo
;M.G. ClementUltimo
2000
Abstract
In anaesthetised, paralysed and mechanically ventilated pigs we evaluated the involvement of ET-1 on PAF-dependent respiratory effects, blocking ET A and ETB receptors with BQ123 and BQ788 respectively. To avoid interference by nitric oxide we used L-NAME, an inhibitor of both NO synthases. The results show that PAF causes a decrease in Crs and an increase in Pmax and Pst, evidencing that the change in Rrs is due to a bron-choconstrictor effect and to a change in viscoelastic properties of the respiratory system. PAF did not significantly affect systemic arterial pressure, while caused a marked increase in mean pulmonary arterial pressure (MPAP). The block of ET-1 receptors partially reduced the respiratory effects elicited by PAF, but did not affect the changes in MPAP. In conclusion our results evidence that PAF favours a release of ET-1. This peptide strengthened PAF-dependent bronchoconstriction and impairs viscoelastic properties of the respiratory system.Pubblicazioni consigliate
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