氧合血红蛋白在自发性蛛网膜下腔出血脑血管痉挛中的作用

目的 研究蛛网膜下腔出血(SAH)后脑脊液中氧合血红蛋白(HbO2)、还原氧合血红蛋白(HbDeoxy)和正铁血红蛋白(HbMet)的浓度随时间变化情况及与脑血管痉挛的关系,并观察SAH后脑动脉血流速度与氧合血红蛋白是否相关。 方法 选择发病后24 h内入院的SAH患者共27例。分别于患者发病的第1、3、5、7、10、14天行腰椎穿刺取脑脊液,离心后取上清液,用紫外分光光度仪测量HbO2、HbDeoxy及HbMet的浓度,所得数据经统计学处理后绘趋势图并进行相关分析,并用经颅多普勒(TCD)对大脑中动脉(MCA)血流速度进行监测。 结果 SAH患者HbO2的浓度在发病第3天开始上升,在第7天达到高峰,为1.4×10-2mmol／L,与第1、3、14天相比,P<0.05;HbDeoxy的浓度在第5天开始上升,在第7天达到高峰5.5×10-3mmol／L,与第1、3、5、14天相比,P<0.05:而HbMet的浓度随时间只是轻度上升,在第14天达到高峰7.5×10-3mmol／L,与其他天相比P>0.05。用TCD测得MCA的血流速度从第5天开始升高,到第7天达到高峰111.2 cm／s。对MCA的血流速度变化与HbO2的浓度变化行相关分析,r=0.906,两者呈正相关。 结论 本研究支持HbO2是引起SAH后慢性脑血管痉挛的主要启动因子之一这一假说,并暗示了HbDeoxy也可能是致挛因子。同时证明了SAH后脑动脉血流速度与HbO2有相关性及TCD在

A study on the effect of oxyhemoglobin in cerebral vasospasm after spontaneous subarachnoid hemorrhage

Objective To investigate the relation between the temporal changes of oxyhemoglobin (HbO2), deoxygemoglobin (HbDeoxy) and methemoglobin(HbMet) concentrations in cerebrospinal fluid and the degree of cerebral vasospasm by observing the relation between the concentrations of the 3 materials after SAH and the velocity of blood in the cerebral arteries detected by TCD. Methods 27 patients admited within 24h after SAH were selected, the CSF of 27 patients were collected by lumber puncture on the 1st, 3rd, 5th, 7th, 10th and 14th day after SAH, the levels of HbO2, HbDeoxy and HbMet were measured by means of spectrophotometry. Detected the velocity of blood flow in MCA by TCD. Results Concentration of HbO2 increased from the 3rd day and peaked on the 7th day in patients after SAH ( P<0. 05) compared with the levels of the 1st, 3rd and 14th day. Concentration of HbDeoxy peaked on the 7th day ( P<0. 05) compared with the levels of the 1st, 3rd, 5th and 14th day. HbMet levels increased only slightly and peaked on the 14th day, compared the other days there was no significant difference ( P>0. 05) . MCA blood flow velocity measured by TCD increased from the 5th day and reached the peak on the 7th day. MCA blood flow velocity showed positive correlation with the level of HbO2 ( r = 0. 906). Conclusion This study showed that the concentration of HbO2 and HbDeoxy increased in CSF during the development of delayed cerebral vasospam. The results supported the hypothesis that HbO2 is involved in the pathogenesis of delayed cerebral vasospam after SAH and suggested that HbDeoxy is a possible vasospastic agent. The study also showed that there was positive correlation between the blood flow velocity and the concentration of HbO2 in CSF after SAH, and the value of TCD in the diagnose of cerebral artery vasospasm.