大鼠蛛网膜下腔出血脑微区血流量与血清一氧化氮变化

目的探讨蛛网膜下腔出血（ＳＡＨ）后继发性脑缺血损害及其一氧化氮（ＮＯ）的作用。方法应用非开颅性方法建立大鼠ＳＡＨ模型，检测２４ｈ内脑微区血流量和颅内血清ＮＯ的动态改变，并测量基底动脉（ＢＡ）管径。结果ＳＡＨ后脑微区血流量迅速降低，１ｈ达最低值，２４ｈ内无明显恢复趋势（Ｐ＜ ０．０１）。ＳＡＨ后１ｈ血清ＮＯ开始减低，井持续２４ｈ（Ｐ＜０．０１）。ＢＡ管径于ＳＡＨ后明显缩小（Ｐ＜０．０１）。结论ＳＡＨ时脑灌注压降低、脑血管痉挛及微循环异常均可能与脑血流量降低有关。ＮＯ减少是脑血管痉挛和微循环异常发生的重要因素之一。

Changes of Microregional Cerebral Blood Flow and Serum Nitric Oxide Content Following Subarachnoid Hemorrhage in Rats

Objective To investigate the secondary brain ischemic damage and the role that nitric oxide plays after subarachnoid hemorrhage (SAH).Methods Noncraniotomy models of SAH in Wistar rats were used to determine the dynamic changes of microregional cerebral blood flow and intracranial serum nitric oxide content within 24h. Diameter of basilar artery was also measured. Results Microregional cerebral blood flow reduced immediately after SAH,reaching its nadir at 1h,maintaining at a lower level within 24h(P<0.01). Serum nitric oxide content decreased from 1h to 24hs after SAH (P< 0.01 ). Diameter of basilar artery reduced significantly 0. 5h after onset of SAH(P<0.01 ). Condusions Reduction of cerebral perfusion pressure,spasm of the cerebral arteries and microcirculatory disturbance may contribute to the decrease of microregional cerebral blood flow following SAN.Reduction of nitric oxide level may be one of the important factors that are responsible for cerebral vasospasm and disturbance of microcirculation.