冠状动脉结扎（孙络疏失）模型大鼠血浆内皮细胞活性因子及微血管舒缩因子的动态变化研究

目的探讨冠状动脉结扎（孙络疏失）模型大鼠血浆血管疏缩因子内皮素-1、血栓素B2、6-酮-前列腺素F1а、血管紧张素Ⅱ的变化规律。方法将心电图正常的60只雄性SD大鼠随机分为假手术组、造模30分钟组、造模1小时组、造模6小时组、造模12小时组、造模24小时组。通过结扎大鼠冠状动脉前降支的方法造成急性心肌缺血模型（＂孙络疏失＂模型）,假手术组只穿线不结扎。放射免疫法检测血浆血管疏缩因子内皮素-1、血栓素B2、6-酮-前列腺素F1а、血管紧张素Ⅱ水平。结果经单因素方差分析LSD检验,与假手术组比较,血浆血管疏缩因子内皮素-1水平在造模1小时组、造模6小时组、造模12小时组显著升高（P〈0.05）,并于24小时恢复正常;血浆6-酮-前列腺素F1а水平在各个模型组均显著下降（P〈0.01或P〈0.05）,于12小时达到最低水平;血浆血栓素B2水平在造模6小时组显著升高（P〈0.01）,而在造模12小时组、造模24小时组明显下降（P〈0.05）;血浆血管紧张素Ⅱ在造模30分钟组、造模1小时组显著降低（P〈0.01或P〈0.05）,于1小时达到最低,而造模6小时组、造模12小时组、造模24小时组则回升至正常水平。结论微血管内皮细胞功能紊乱导致的微血管舒缩因子异常分泌、动态平衡遭到破坏,在＂孙络疏失＂急性期的病理变化过程中发挥重要作用。

Dynamic alterations of TXB 2,6-keto-PGF 1α,ET-1 and AngⅡin modeled rats with coronary artery ligation（the pattern of loosened and weakened minute collaterals in the domain of Chinese medicine）：An observational study

Objective To explore the way how endothelin-1（ ET-1）,thromboxaneB 2（ TXB 2）,6-keto-prostaglandin1α（ PGF1α） and angiotensinⅡ（ AngⅡ） changes in modeled rats with coronary artery ligation（ the pattern of loosened and weakened minute collaterals in the domain of Chinese medicine）. Methods A total of 60 male Sprague-Dawley rats with regular ECG performance were randomized into Sham-operation group,30min-modeling group,a 1h-modeling group,a 6h-modeling group,a 12h-modeling group and a 24h-modeling group. The model of loosened and weakened minute collaterals in heart was established after ligation of the left anterior descending coronary artery,while the sham group was punctured without ligation. The level of plasma ET-1,TXB 2,6-Keto-PGFla and AngⅡ were detected with radioimmunoassay. Results Compared with the sham group,the ET-1 levels in the 1h-modeling group,the 6hmodeling group and the 12h- modeling group were significantly increased（ P ＆lt; 0. 05）,then returned to nomal states at 24h. The TXB 2 levels were obviously increased in the 6h- modeling group（ P ＆lt; 0. 01）, while decreased apparently at the 12h- modeling group and the 24h- modeling group（ P ＆lt; 0. 05）. The 6-keto-PGFlα levels in all the model groups were significantly decreased（ P ＆lt; 0. 01 or P ＆lt; 0. 05）,then reached the lowest peak at 12h. The AngⅡ levels in the 30min-group and the 1h-group were obviously decreased（ P ＆lt; 0. 01 or P ＆lt; 0. 05）,then reached the low peak at 1h,while returned to nomal level in the 6hmodeling group,the 12h- modeling group and the 24h- modeling group. Conclusions The abnormal expression of vasomotor activity factor accompanies with the dynamic equilibrium destruction,due to the dysfunction of microvascular endothelial cell,and it exerts an important effect during the process of pathological change in acute phase of loosened and weakened minute collaterals.