AIM: To investigate the changes of somatosensory evoked potential(SEP), nitric oxide (NO) levels both in serum and in brain tissue after subarachnoid hemorrhage(SAH) and the influence of Ginkgo biloba extract(GBE) on them. METHODS: Wistar rats were divided into sham-operated group, pure SAH group and GBE-treated group. Dynamic changes of regional cerebral blood flow( rCBF),SEP, and NO levels both in serum and in brain tissue were detected within 24 hours after operation. RESULTS: In pure SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24 hours. Latency of SEP delayed progressively from 1 hour to 24 hours after SAH.NO levels in serum and in brain tissue decreased and increased respectively from 1 hour to 24 hours after SAH. GBE effectively antagonized the changes of above parameters. CONCLUSION: SEP is useful in the judgement of cerebral ischemic damage after SAH. Decrease of serum NO and increase of brain NO are important factors leading to cerebral vasospasm and neural damage respectively after SAH. GBE relieves cerebral ischemic damage by reversing the pathological alterations of NO.

AIM: To investigate the changes of somatosensory evoked potential(SEP), nitric oxide (NO) levels both in serum and in brain tissue after subarachnoid hemorrhage(SAH) and the influence of Ginkgo biloba extract(GBE) on them. METHODS: Wistar rats were divided into sham-operated group, pure SAH group and GBE-treated group. Dynamic changes of regional cerebral blood flow( rCBF),SEP, and NO levels both in serum and in brain tissue were detected within 24 hours after operation. RESULTS: In pure SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24 hours. Latency of SEP delayed progressively from 1 hour to 24 hours after SAH.NO levels in serum and in brain tissue decreased and increased respectively from 1 hour to 24 hours after SAH. GBE effectively antagonized the changes of above parameters. CONCLUSION: SEP is useful in the judgement of cerebral ischemic damage after SAH. Decrease of serum NO and increase of brain NO are important factors leading to cerebral vasospasm and neural damage respectively after SAH. GBE relieves cerebral ischemic damage by reversing the pathological alterations of NO.

AIM: To investigate the role of nitric oxide in the development of brain edema after subarachnoid hemorrhage(SAH), and the influence of L-arginine on them. METHODS: Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group, SAH group and SAH plus L-arginine group. Dynamic changes of regional cerebral blood flow within 24 hours were measured. Serum nitric oxide level, brain water and sodium content at different time points within 24 hours were also detected. RESULTS: Regional cerebral blood flow and serum nitric oxide level at every time point after operation in SAH group were lower than those in sham-operated group, while brain water content and sodium content in the former group were higher than those in the latter group. Above pathological alterations in SAH plus L-arginine group were not so obvious as in SAH group. CONCLUSION: Decrease in serum nitric oxide plays a role in the development of brain edema after SAH, which may be partly reversed by administration of L-arginine.

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.