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目的:探讨冠心病心绞痛寒凝血瘀证与血管内皮功能的相关性。方法:采用垂体后叶素大剂量静脉注射建立冠心病心绞痛寒凝血瘀证动物模型,检测模型大鼠血管活性物质ET-1、NO、TXB2、6-Keto-PGF1α水平的变化。结果:模型组大鼠血ET-1、NO、TXB2水平显著升高,6-Keto-PGF1α水平降低,TXB2/6-Keto-PGF1α值显著升高,与正常组相比差异有统计学意义(P<0.05或P<0.01)。结论:血管活性物质失衡参与了冠心病心绞痛寒凝血瘀证的病理变化过程,血管内皮功能紊乱主导了寒凝血瘀证的内在病理机制,冠心病心绞痛寒凝血瘀证与血管内皮功能紊乱密切相关。
Objective: To investigate the correlation between coronary heart disease and angina pectoris blood coagulation syndrome and vascular endothelial function. Methods: The animal model of coronary heart disease with cold coagulation and blood stasis was established by intravenous administration of high dose of vasopressin. The levels of ET-1, NO, TXB2, 6-Keto-PGF1α in the model rats were measured. Results: The levels of ET-1, NO and TXB2 in the model group were significantly increased, the level of 6-Keto-PGF1α was decreased and the level of TXB2 / 6-Keto-PGF1α was significantly increased compared with the normal group P <0.05 or P <0.01). CONCLUSION: The imbalance of vasoactive substances is involved in the pathological changes of blood coagulation and blood stasis syndrome of angina pectoris. Endothelial dysfunction dominates the pathological mechanism of cold coagulation and blood stasis syndrome. The coronary heart disease angina pectoris coagulation and blood stasis syndrome is closely related to vascular endothelial dysfunction.