【摘要】 【目的】探讨急性脑损伤后心肌损害、血浆和心肌局部血管紧张素Ⅱ及其受体的变化以及预先应用血管紧张素受体阻断剂对其的影响。【方法】建立颅脑损伤及血管紧张素受体阻滞剂(ARB)药物干预模型,测定血浆AngⅡ水平和血清肌酸磷酸激酶同工酶含量,免疫组织化学方法检测心肌AngⅡ和血管紧张素受体1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,HE染色和超微结构的病理观察可见心肌损害。预先应用ARB心肌组织AT1R表达及血清CK-MB水平比单纯损伤大鼠显著降低,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。ARB具有防止颅脑损伤后心肌损害的作用。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。更多还原

【Abstract】 [Objective]To determine myocardial damage,changes of plasma,myocardial angiotensin Ⅱ and myocardial AT1 receptor as well as effects of Angiotensin ⅡSubtype 1 Receptor Blocker (ARB) after brain injury in rats. [Methods]Brain injury was induced by weight-drop technique and pretreated by ARB. 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 ARB group comparing with brain injury group. Relief of myocardial damage was also observed with light and electronic microscope in ARB group. [Conclusions]Brain injury can lead to myocardial damage. Rennin-Angiotensin System (RAS) maybe plays an important role in the mechanism of myocardial damage after brain injury. ARB can prevent myocardial damage after brain injury.更多还原