论文部分内容阅读
目的探讨一氧化氮（ＮＯ）与蛛网膜下腔出血（ＳＡＨ）后缺血性脑损害的关系和银杏叶制剂（ＧＢＥ）的保护作用。方法应用非开颅大鼠模型，对ＳＡＨ组和ＧＢＥ组测量基底动脉（ＢＡ）管径并观察２４ｈ内微区脑血流量（ＣＢＦ）和颅内血清ＮＯ水平动态改变，３ｄ后对海马ＣＡ１区行病理检查。结果ＳＡＨ后ＣＢＦ和血清ＮＯ降低，ＢＡ痉挛，海马ＣＡ１区神经元明显受损。ＧＢＥ使上述改变减轻。结论ＳＡＨ时血清ＮＯ减少是导致缺血性脑损害的重要因素，ＧＢＥ通过影响ＮＯ病理性改变而减轻缺血性脑损害
Objective To investigate the relationship between nitric oxide (NO) and ischemic brain damage after subarachnoid hemorrhage (SAH) and the protective effect of Ginkgo biloba preparation (GBE). Methods Non-craniotomy rats were used to measure the diameter of basilar artery (BA) in SAH group and GBE group. The changes of micro-regional cerebral blood flow (CBF) and intracranial serum NO level in 24h were observed. Pathological examination. Results After SAH, CBF and serum NO decreased, BA spasm, hippocampal CA1 neurons were significantly impaired. The GBE mitigates these changes. Conclusions The decrease of serum NO in SAH is an important factor leading to ischemic brain damage. GBE can reduce ischemic brain damage by affecting the pathological changes of NO