M. Clement et M. Albertini, ROLE OF ENDOGENOUS NITRIC-OXIDE ON PAF-INDUCED VASCULAR AND RESPIRATORY EFFECTS, Mediators of inflammation, 4(2), 1995, pp. 124-129
THE role of endogenous nitric oxide (NO) on vascular and respiratory s
mooth muscle basal tone was evaluated in six anaesthetized, paralysed,
mechanically ventilated pigs. The involvement of endogenous NO in PAF
-induced shock and airway hyperresponsiveness was also studied. PAF (5
0 ng/kg, i.v.) was administered before and after pretreatment with N-G
-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg, i.v.), an NO synthes
is inhibitor. PAF was also administered to three of these pigs after i
ndomethacin infusion (3 mg/kg, i.v.). in normal pigs, L-NAME Increased
systemic and pulmonary vascular resistances, caused pulmonary hyperte
nsion and reduced cardiac output and stroke volume. The pulmonary vasc
ular responses were correlated with the increase in static and dynamic
lung elastances, without changing lung resistance. Inhibition of NO s
ynthesis enhanced the PAF-dependent increase in total, intrinsic and v
iscoelastic lung resistances, without affecting, lung elastances or ca
rdiac activity. The systemic hypotensive effect of PAF was not abolish
ed by pretreatment with L-NAME or indomethacin. This indicates that sy
stemic hypotension is not correlated with the release of endogenous NO
or prostacyclines. Indomethacin completely abolished the PAF-dependen
t respiratory effects.