论文部分内容阅读
目的:探讨丹参注射液对兔急性心肌梗死后梗死及其周围区血管再生的影响。方法:用开胸结扎冠状动脉左室支的方法建立急性心肌梗死模型,将已建立心肌梗死模型的日本大耳白兔随机分为模型对照组(B)、丹参组(C)。急性心肌梗死术后C组静脉推注丹参注射液10日。术后5周处死动物,取梗死及其周围区组织,(1)对梗死及其周围区进行血小板内皮细胞黏附分子-1(CD31)免疫组化染色,以观察毛细血管密度;(2)对梗死及其周围区进行血管内皮生长因子(VEGF)免疫组化染色,进一步探究丹参注射液促进血管生成的机制。结果:(1)梗死及其周围区CD31的表达,正常组和中药丹参组均高于模型组(P<0.05),正常组高于中药丹参组(P<0.05)。(2)梗死及其周围区VEGF的表达,丹参组高于模型组和正常组(P<0.05)。结论:中药丹参可促进兔心肌梗死后梗死区毛细血管新生,增加梗死及其周围区血管数量来改善心肌梗死后梗死及其周围区的供血以改善微循环,从而减少心肌梗死的面积,改善预后,其机制可能是通过提高梗死及其周围区VEGF的表达而实现的。
Objective: To investigate the effect of Salvia miltiorrhiza injection on revascularization of infarct and its surrounding area after acute myocardial infarction in rabbits. METHODS: An acute myocardial infarction model was established by ligation of the left ventricle of the coronary artery with a thoracotomy. Japanese rabbits with established myocardial infarction models were randomly divided into model control group (B) and Salvia miltiorrhiza group (C). After acute myocardial infarction, C group was injected with Danshen injection intravenously for 10 days. The animals were sacrificed 5 weeks after surgery, and the infarct and its surrounding tissues were taken. (1) The platelet endothelial cell adhesion molecule-1 (CD31) immunohistochemical staining was performed on the infarct and its surrounding area to observe the capillary density; (2) Immunohistochemical staining of vascular endothelial growth factor (VEGF) was performed in the infarct and its surrounding area to further explore the mechanism of Danshen injection in promoting angiogenesis. Results: (1) The expression of CD31 in the infarct and its surrounding area was higher in the normal group and the Salvia miltiorrhiza group than in the model group (P<0.05), and higher in the normal group than in the Salvia miltiorrhiza group (P<0.05). (2) The expression of VEGF in infarct and its surrounding area was higher in Danshen group than in model group and normal group (P<0.05). Conclusion: Salvia miltiorrhiza can promote capillary angiogenesis in infarcted area after myocardial infarction in rabbits, increase the number of blood vessels in infarct and its surrounding area to improve the blood supply of infarct and its surrounding areas after myocardial infarction to improve microcirculation, thereby reducing the area of myocardial infarction and improving prognosis. The mechanism may be achieved by increasing the expression of VEGF in the infarct and its surrounding area.