摘要
目的 探讨叔丁基氢过氧化物 (t BHP)及低氧在诱导小鼠短暂性脑缺血样发作 (TIA like)中的作用及关系。方法 将 5 6只昆明小鼠随机分成A(生理盐水对照组 )、B(t BHP组 )、C (t BHP +低氧组 )、D(模型组 ) 4组。先将D组小鼠由尾静脉注射t BHP(0 11mol/L、10ml/kg) ,每次间隔 2 4h,诱导小鼠TIA like。D组出现TIA like的时间为 (3 7± 1 1)d ,以此作为实验采血时间的依据 ,观察其他各组在不同诱发条件下TIA like前血液流变学变化。结果 与A组比较 ,B、C两组在高、低切变率下全血黏度、纤维蛋白原 (Fg)均明显升高 (均P <0 .0 1) ,低氧没有进一步增加血黏度及血Fg含量 (P >0 .0 5 ) ,但可增强t BHP在诱导TIA like中的作用。结论 t BHP可导致血黏度增高、脑微循环功能障碍 ;低氧可能通过t BHP对血管内皮细胞的损伤 ,导致血管代偿调节能力减弱而增强t
Objective To explore the effects and relationship of tert-butyl hydroperoxide (t-BHP) and hypoxia in transient ischemia-like attack (TIA-like) in Kunming mice.Methods Fifty-six mice were randomly divided into normal saline group (group A), t-BHP group (group B), t-BHP plus hypoxia group (group C) and model group (group D). Fourteen mice in group D were injected t-BHP (0.11 mol/L, 10 ml/kg) through tail vein with an interval of 24 hrs to induce TIA-like attack. The average time of TIA-like was ( 3.7± 1.1) days, and this time was used as experimental evidence to collect blood sample in other groups. Hemorheological indexes before TIA-like attack were observed in different experimental conditions.Results Compared with group A, the whole blood viscosity at shear rate 100S-1, 1S-1 and Fibrinogen were significantly increased in group B and group C (all P<0.01). Hypoxia did not deteriorate blood viscosity and Fibrinogen but enhanced TIA-like attack induced by t-BHP.Conclusions t-BHP may increase whole blood viscosity and lead to dysfunction of cerebral microcirculation. It is likely that hypoxia damages vascular endothelium and weakens vascular compensation ability to enhance the effect of t-BHP.
出处
《临床神经病学杂志》
CAS
2004年第6期444-445,共2页
Journal of Clinical Neurology
基金
江苏省卫生厅基金资助 (H 9746)
徐州市科委基金资助 (X 9877)
