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Aim: To investigate the changes of nitric oxide and endothelin-1 levels in brain tissue in rat with cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH), and the protective effect of nimodipine., Methods: Wistar rats were divided randomly into SAH group, nimodipine-treated group and sham-operated group. Diameters of basilar artery before and after operation were measured, and dynamic changes of regional cerebral blood flow (rCBF), brain nitric oxide and endothelin-1 levels were determined within 24 h. Pathological examination of hippocampus was also performed., Results: SAH resulted in significant and persistent decrease of rCBF. Diameter of basilar artery was reduced markedly. Neurons in hippocampus CA1 subfield were damaged severely. Both nitric oxide and endothelin-1 levels in brain tissue were increased significantly from 1 h to 24 h after SAH. However, the pathological changes of above parameters were not so severe in nimodipine-treated rats., Conclusion: Increase of nitric oxide and endothelin-1 levels in brain tissue is probably involved in the development of ischemic brain damage caused by CVS after SAH. Nimodipine exerts its protective effect on brain neurons by antagonizing CVS and the pathological changes of nitric oxide and endothelin-1 in brain tissue.

Objective: To observe the changes of somatosensory evoked potential(SEP) and nitric oxide (NO) after subarachnoid hemorrhage(SAH), and the influence of Ginkgo biloba extract (EGb)., Method: Rats in sham-operated group, SAH model group and EGb-treated group underwent measurement of dynamic changes of regional cerebral blood flow(rCBF), SEP and NO levels both in serum and in brain tissue within 24 h after operation., Result: In SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24 h. The latency of SEP delayed progressively from 1 h to 24 h after SAH. NO levels in serum and in brain tissue decreased and increased respectively from 1 h to 24 h after SAH. EGb effectively antagonized the changes of above parameters., Conclusion: SEP is helpful in the judgement on brain ischemic damage after SAH. Decrease of NO in serum and increase of that in brain tissue may lead to cerebral vasospasm and ischemic brain damage respectively after SAH. EGb relieves SAH-induced brain ischemic damage by reversing the pathological alterations of NO.

This study aimed to investigate the protective effects of Ginkgo biloba extract on cerebral vasospasm and neural damage following subarachnoid hemorrhage (SAH) in rats. It was found that the regional cerebral blood flow decreased immediately and persistently after SAH in SAH rats. The latency of somatosensory evoked potential delayed progressively. The nitric oxide levels in serum and brain tissue decreased and increased, respectively, after SAH. Ginkgo biloba extract effectively antagonized the changes of above parameters. It was concluded that somatosensory evoked potential is useful for the judgement of cerebral ischemic damage during cerebral vasospasm after SAH. Decrease in serum nitric oxide and increase in brain tissue nitric oxide are important factors leading to cerebral vasospasm and neural damage, respectively, after SAH. Ginkgo biloba extract relieves cerebral vasospasm and cerebral ischemic damage by reversing the pathological alteration of nitric oxide.