蛛网膜下腔出血并迟发性脑血管痉挛大鼠脑能量代谢与脑血流量变化的实验研究

目的探讨实验性蛛网膜下腔出血导致的迟发性脑血管痉挛时脑能量代谢的变化规律，及其与皮质脑血流量（CBF）变化的相关性。方法50只雄性SD大鼠随机分为对照组和蛛网膜下腔出血第1、3、5、7天组．应用非抗凝自体动脉血枕大池两次注血法制备蛛网膜下腔出血大鼠模型；另5只大鼠用于颅内血液大体分布的观察。应用微透析仪监测各组大鼠脑组织间液中葡萄糖（Glu）、乳酸（Lac）及丙酮酸（Pyr）含量，并计算乳酸／丙酮酸比值；激光多普勒血流仪监测各组大鼠皮质脑血流量；于光学显微镜及透射电子显微镜下观察基底动脉血管壁的病理学改变。结果（1）5只用于观察颅内血液大体分布的大鼠中4只蛛网膜下腔出血模型鼠血液主要分布于基底池、脚间池及额叶底面，亚甲蓝与血液混合物主要沉积于颅底．同时在脑室及纵裂池亦可见血液分布；余1只注入人工脑脊液后未发生颅内出血及血液沉积。表明蛛网膜下腔出血动物模型制备成功。（2）与对照组相比，蛛网膜下腔出血组大鼠葡萄糖及丙酮酸含量明显降低（P〈0．01）；乳酸／丙酮酸比值明显升高（P〈0．01），以第5、7天组升高最为明显（P〈0．01）；第5天组乳酸含量亦明显升高（P〈0．01）。（3）激光多普勒监测显示，蛛网膜下腔出血组大鼠脑血流量减少率高于对照组（P〈0．05），其中第5天组减少最为显著。与其他各亚组比较差异有统计学意义（尸〈0．05）；脑血流量变化与乳酸／丙酮酸比值、乳酸水平的改变呈正相关（r=0．721，0．477；均P〈0．01），与葡萄糖、丙酮酸水平的改变呈负相关（r=-0．447，-0．579；均P〈0．01）。结论微透析指标与脑血流量变化具有一致性，可作为蛛网膜下腔出血脑组织间液生化指标的动态监测，用于预测迟发性脑血管痉挛的发生。

Experimental study on the correlation between the cerebral energy metabolism and cerebral blood flow changes in rats with subarachnoid hemorrhage-induced delayed cerebral vasospasm

Objective To explore the changes of the cerebral energy metabolism in rats with experimental subarachnoid hemorrhage (SAH)-induced delayed cerebral vasospasm, and the correlation with cerebral blood flow (CBF) changes. Methods Male Sprague-Dawley rats (n = 50) were randomly divided into five groups: control group and 1 d, 3 d, 5 d and 7 d SAH group. The animal model was prepared by two injections of nonheparinized autologous arterial blood into the cisterna magna. Another 5 rats were used to observe intracranial blood distribution. Microdialysis (MD) was applied to monitor the levels of glucose (Glu), lactic acid (Lac), pyruvic acid (Pyr) in the cerebral extracellular fluid (ECF) in each group, and calculated the ratio of Lac and Pyr. The cortical CBF was measured by Laser Doppler Flowmetry (LDF). Histopathological changes of the basilar artery wall were observed by light microscope and transmission electron microscope. Results 1) In 5 rats for observing intracranial blood distribution, the blood of 4 SAH models was distributed mainly in basal cistern, interpeduncular cistern and the basis of frontal lobe. The mixture of methylene blue and blood was mainly deposited at the base of skull, and blood was distributed in cerebral ventricules and longitudinal fissure cistern. In the rest one as a control which was injected with artificial cerebrospinal fluid, no intracranial hemorrhage and blood deposition were seen. It indicated that SAH model was successively prepared. 2) In comparison with the control group, levels of Glu and Pyr decreased significantly (P < 0.01) and Lac/Pyr ratio increased significantly (P < 0.01) in SAH rats while the increase of Lac/Pyr ratio was most remarkable in 5 d group and 7 d group (P < 0.01). The increase of Lac level was also significant in 5 d group (P < 0.01). 3) In the monitor of LDF, the CBF reduction rates in SAH groups were higher than that in control group (P < 0.05), and the reduction in 5 d group was most significant in comparison with other subgroups (P < 0.05). The changes in CBF was positively correlated with Lac/Pyr ratio and Lac level (r = 0.721, 0.477; P < 0.01, for all), but was negatively correlated with Glu level and Pyr level (r = - 0.447, - 0.579; P < 0.01, for all). Conclusion MD indexes are consistant with CBF changes. It can be used as a dynamic monitor to indicate the biochemical index of cerebral interstitial fluid in SAH, and can be also used for predicting the onset of delayed cerebral vasospasm.