RESUMO
AIM: To investigate the role of nitric oxide in neuronal damage induced by cerebral vasospasm (CVS) following subarachnoid he morrhage (SAH) in rats. METHODS: Noncraniotomy models of SAH by a endovascular puncture method in Wistar rats were used and animals were divided i nto sham-operated group, SAH group and SAH+L-arginine group. Dynamic changes of regional cerebral blood flow (rCBF) within 24 hours were monitored. Diameters of basilar artery (BA) were measured. Serum NO(NO - 2/NO - 3) and plasma endo thelin-1 content at different time points within 24 hours were also detected. RESULTS: Sham operation did not affect all of above parameters. In SAH group, rCBF reduced immediately after induction of SAH, reaching its lowe st at 1 h, persisting within 24 h. Diameter of BA significantly decreased after S AH. Serum NO - 2/NO - 3 decreased and plasma endothlin-1 increased statisti cally after SAH. In SAH+L-arginine group, decline of rCBF was not as rapid and s evere as that in SAH group. L-arginine also effectively antagonized vasospasm of BA and damage of hippocampal neurons. Decrease of serum NO - 2/NO - 3 and increase of plasma endothlin-1 were not so obvious in SAH+L-arginine group comp ared to SAH group. CONCLUSION: Decrease in NO is involved in the development of CVS- induced neuronal damage following SAH, and L-arginine partly increases serum NO and thus protectes ischemic brain neurons.