论文部分内容阅读
目的 :建立SD大鼠血管内皮细胞损伤动物模型。方法 :SD大鼠随机分为正常对照组和模型组。模型组大鼠皮下注射稀释 1.5倍的肾上腺素 0 .0 5 / 10 0 g ,连续 5天。于第 4天起 ,每二次给药中间时间将大鼠置于 0℃冰水中 5min ,共 4次。正常对照组则皮下注射等量 0 .9%NS。于第 6天 ,二组大鼠自颈总动脉取血 ,分别测定CEC计数、t PA、PAI活性、6 Keto PGF1α含量及血小板最大聚集率。结果 :模型组较正常对照组大鼠CEC计数、PAI活性、血小板最大聚集率明显升高 (P <0 .0 0 1～ 0 .0 1) ,t PA活性、6 Keto PGF1α含量降低 (P <0 .0 1～ 0 .0 5 )。结论 :大剂量肾上腺素加冰泳刺激确能造成SD大鼠血管内皮细胞损伤。
Objective: To establish an animal model of vascular endothelial cell injury in SD rats. Methods: SD rats were randomly divided into normal control group and model group. Rats in the model group were subcutaneously injected with 1.5-fold diluted epinephrine (0.050 / 10 g) for 5 consecutive days. On day 4, rats were placed in ice-water at 0 ° C for 5 minutes for 4 times each time during the second administration. The normal control group was injected subcutaneously with 0.9% NS. On the 6th day, the rats in the two groups were taken blood from the common carotid artery to measure the CEC count, t PA, PAI activity, 6 Keto PGF1α content and the maximum platelet aggregation rate. Results: Compared with the normal control group, the CEC count, the PAI activity, the maximum platelet aggregation rate and the activity of t PA and the content of 6 Keto PGF1α in model group were significantly decreased (P <0.01. 0 .0 1 ~ 0 .0 5). Conclusion: High-dose epinephrine plus ice-cold stimulation can cause vascular endothelial cell injury in SD rats.