IMPAIRED ENDOTHELIUM-DEPENDENT RELAXATION IN RABBIT PULMONARY-ARTERY AFTER SUBARACHNOID HEMORRHAGE

We investigated the changes in endothelial function of pulmonary as we ll as basilar artery after experimental subarachnoid hemorrhage (SAH) induced by cisternal blood injection in rabbits. The animals were kill ed on day 2 and day 7, and the mechanical responses were determined on transverse strips of the main pulmonary artery and rings harvested fr om the basilar artery. To examine the role of the vagal nerve, we cut the left vagal nerve immediately before injecting cisternal blood. Rel axation response of pulmonary and basilar arteries to acetylcholine (A Ch) and A23187 were abolished after endothelial removal and reatly inh ibited by either N-G-nitro-L-arginine (NOARG) or methylene blue (MB). Indomethacin failed to modify these relaxation responses. Relaxation r esponse of the main pulmonary artery strips to ACh was significantly ( p < 0.05 and p < 0.01) attenuated on day 2 in 6 of 12 rabbits. In the remaining 6 rabbits, relaxation was not affected. No change in relaxat ion responses to A23187 and sodium nitroprusside (SNP) was observed in any of the 12 cases. In the vagotomized rabbits, no decreased respons e to ACh was observed. On day 7, relaxation response to ACh returned t o normal. ACh also produced decreased relaxation in basilar artery rin gs on day 2 with no change in A23187- and SNP-induced relaxation. Cont ractile responses of pulmonary and basilar arteries to norepinephrine (NE), endothelin-1 (ET-1), 5-hydroxytryptamine (5-HT), and U46619 were not affected after SAH. These results suggest that less functional mu scarinic receptors that produce/release less endothelium-derived relax ing factor [EDRF/nitric oxide (NO)] are involved in causing the reduce d relaxation of pulmonary and basilar arteries after SAH and the vagal nerve may play a role in regulating the receptor-mediated, endotheliu m-dependent relaxation in the main pulmonary artery after experimental SAH.