2000Journal of Taishan Medical CollegeRequires access

Changes of latency of somatosensory evoked potential and influence of nimodipine during cerebral vasospasm following subarachnoid hemorrhage

Sun Bao

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Abstract

Objective: To investigate the changes of latency of somatoevoked potential(SEP) and influence of nimodipine during cerebral vasospasm following subarachnoid hemorrhage(SAH). Methods: Rats were divided into pure SAH group and nimodpine treated group. Diameters of basilar artery before and 0.5 h after operation were measured, and dynamic changes of regional cerebral blood flow (rCBF), SEP, endothelin 1 levels in brain tissue within 24 h were determined. Results: In SAH group, diameter of basilar artery was decreased markedly. rCBF was reduced immediately after SAH and retained in 24 h. Latency of SEP was delayed from 1h to 24 h, and endothelin 1 in brain tissue was increased simultaneously. Nimodipine significantly antagonized pathological alterations of above parameters. Conclusion: Cerebral vasospasm after SAH leads to neurological deficit which may be alleviated by nimodipine via antagonizing the pathological alterations of endothelin 1 in brain tissue.

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Objective: To investigate the changes of latency of somatoevoked potential(SEP) and influence of nimodipine during cerebral vasospasm following subarachnoid hemorrhage(SAH). Methods: Rats were divided into pure SAH group and nimodpine treated group. Diameters of basilar artery before and 0.5 h after operation were measured, and dynamic changes of regional cerebral blood flow (rCBF), SEP, endothelin 1 levels in brain tissue within 24 h were determined. Results: In SAH group, diameter of basilar artery was decreased markedly. rCBF was reduced immediately after SAH and retained in 24 h. Latency of SEP was delayed from 1h to 24 h, and endothelin 1 in brain tissue was increased simultaneously. Nimodipine significantly antagonized pathological alterations of above parameters. Conclusion: Cerebral vasospasm after SAH leads to neurological deficit which may be alleviated by nimodipine via antagonizing the pathological alterations of endothelin 1 in brain tissue.

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Available abstract

Objective: To investigate the changes of latency of somatoevoked potential(SEP) and influence of nimodipine during cerebral vasospasm following subarachnoid hemorrhage(SAH). Methods: Rats were divided into pure SAH group and nimodpine treated group. Diameters of basilar artery before and 0.5 h after operation were measured, and dynamic changes of regional cerebral blood flow (rCBF), SEP, endothelin 1 levels in brain tissue within 24 h were determined. Results: In SAH group, diameter of basilar artery was decreased markedly. rCBF was reduced immediately after SAH and retained in 24 h. Latency of SEP was delayed from 1h to 24 h, and endothelin 1 in brain tissue was increased simultaneously. Nimodipine significantly antagonized pathological alterations of above parameters. Conclusion: Cerebral vasospasm after SAH leads to neurological deficit which may be alleviated by nimodipine via antagonizing the pathological alterations of endothelin 1 in brain tissue.

Key concepts: Nimodipine, Subarachnoid hemorrhage, Medicine, Basilar artery, Cerebral vasospasm, Vasospasm, Anesthesia, Cerebral blood flow

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