In 12 anesthetized, paralyzed and mechanically ventilated pigs, the effects of both endogenous and inhaled nitric oxide (NO, 80 ppm for 6 min), have been evaluated in control conditions and after administration of 50 ng/kg i.v. of platelet activating factor (PAF). To study the effects of endogenous NO, NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v.), an inhibitor of NO synthesis, was used. In control conditions, the block of endogenous NO increased pulmonary arterial pressure (PAPM), without changing systemic arterial pressure (PAM) or resistances (Rrs) and compliance (Crs) of the respiratory system. PAF administration causes a pulmonary hypertension and a prompt and brief decrease in systemic arterial pressure. L-NAME administration strengthened the effects of PAF on Rrs, Crs and PAM, while caused a lesser increase in pulmonary arterial pressure. These data show that PAF-dependent systemic hypotension is not caused by endogenous NO and that PAF administration favors the release of NO, which counterbalances the respiratory effects. Inhaled NO, in all experimental conditions, did not modify PAM, while in control conditions caused a decrease in PAPM. Inhalation of NO counterbalanced the respiratory and circulatory effects caused by PAF administration.
Effetti dell’ossido d’azoto (NO) endogeno ed inalato in un modello sperimentale di ipertensione polmonare e broncocostrizione / M. Albertini. - In: ACTA MEDICA VETERINARIA. - ISSN 0001-6136. - 42:1/2(1996), pp. 61-70.
Effetti dell’ossido d’azoto (NO) endogeno ed inalato in un modello sperimentale di ipertensione polmonare e broncocostrizione
M. AlbertiniPrimo
1996
Abstract
In 12 anesthetized, paralyzed and mechanically ventilated pigs, the effects of both endogenous and inhaled nitric oxide (NO, 80 ppm for 6 min), have been evaluated in control conditions and after administration of 50 ng/kg i.v. of platelet activating factor (PAF). To study the effects of endogenous NO, NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v.), an inhibitor of NO synthesis, was used. In control conditions, the block of endogenous NO increased pulmonary arterial pressure (PAPM), without changing systemic arterial pressure (PAM) or resistances (Rrs) and compliance (Crs) of the respiratory system. PAF administration causes a pulmonary hypertension and a prompt and brief decrease in systemic arterial pressure. L-NAME administration strengthened the effects of PAF on Rrs, Crs and PAM, while caused a lesser increase in pulmonary arterial pressure. These data show that PAF-dependent systemic hypotension is not caused by endogenous NO and that PAF administration favors the release of NO, which counterbalances the respiratory effects. Inhaled NO, in all experimental conditions, did not modify PAM, while in control conditions caused a decrease in PAPM. Inhalation of NO counterbalanced the respiratory and circulatory effects caused by PAF administration.Pubblicazioni consigliate
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