【摘要】 目的探讨血管紧张素转化酶抑制剂(ACEI)对颅脑损伤大鼠心肌损害、循环和心肌局部血管紧张素Ⅱ(AngⅡ)及其受体的影响。方法建立颅脑损伤及ACEI药物干预大鼠模型,测定大鼠血浆AngⅡ水平和血清肌酸磷酸激酶同工酶(CK-MB)含量,免疫组化方法检测心肌AngⅡ和血管紧张素受体1(AT1R)表达,并观察心肌HE染色及超微结构病理形态学改变。结果大鼠颅脑损伤后血浆AngⅡ、心肌组织AngⅡ和AT1R水平显著升高,血清CK-MB含量显著增高(P<0.05或<0.01),HE染色和超微结构的病理观察可见心肌损害;ACEI干预组血浆和心肌AngⅡ含量及血清CK-MB水平较单纯损伤组显著降低,HE染色和超微结构可见心肌损伤程度减轻。结论颅脑损伤可引起明显的心肌损害,肾素—血管紧张素系统可能是参与颅脑损伤后心肌损害的机制之一;ACEI具有防止颅脑损伤后心肌损害的作用。更多还原

【Abstract】 Objective To determine the effect of ACEI on myocardial damage,the changes of plasma,myocardial angiotensinⅡ and myocardial AT1 receptor after brain injury in rats.Methods Brain injury was induced by weight-drop technique and pretreated by ACEI.Plasma angiotensinⅡ level was determined using RIA.Myocardial angiotensinⅡand AT1 receptor were detected by immunohistochemical method.Myocardium-type creatine kinase isoenzyme(CK-MB) was measured.The morphologic changes of myocardium were observed with light and electronic microscope.Results Plasma angiotensin Ⅱ and serum CK-MB increased 24 hours after brain injury.AngiotensinⅡand AT1 receptor in myocardium also increased.Degeneration and necrosis of myocardium were detected with light and electronic microscope,which included increasing and swelling of mitochondria and disruption of cardiac muscle fiber.Plasma angiotensin Ⅱ and serum CK-MB decreased in ACEI group comparing with brain injury group.Relief of myocardial damage was also observed with light and electronic microscope in ACEI group.Conclusion Brain injury can lead to myocardial damage.Rennin-angiotensin system maybe play an important role in the mechanism of myocardial damage after brain injury.ACEI can prevent myocardial from damage after brain injury.更多还原