大鼠颅脑损伤后血管紧张素及其受体变化与B受体阻断剂对其的影响

首都医科大学学报 ›› 2005, Vol. 26 ›› Issue (3): 299-302.

大鼠颅脑损伤后血管紧张素及其受体变化与B受体阻断剂对其的影响

郭彩霞¹, 杜凤和¹, 张立克², 陈瑞芬², 孙异临³

1. 首都医科大学附属北京天坛医院心血管内科;2. 首都医科大学基础医学院;3. 首都医科大学附属北京天坛医院电镜室

收稿日期:2004-11-30 修回日期:1900-01-01 出版日期:2005-06-24 发布日期:2005-06-24

Myocardial Damage, Alterations of Angiotensin and Receptors after BrainInjury in Rats and Preconditional Effects of Bisoprolol on Them

Guo Caixia¹, Du Fenghe¹, Zhang Like², Cheng Ruifen², Sun Yilin³

1. Department of Cardiology Medicine, Beijing Tiantan Hospital, Capital University of Medical Sciences;2. School of Basic Sciences, Capital University of Medical Sciences;3. Department of Electron Microscope, Beijing Tiantan Hospital, Capital University of Medical Sciences

Received:2004-11-30 Revised:1900-01-01 Online:2005-06-24 Published:2005-06-24

摘要/Abstract

摘要：

目的探讨颅脑损伤后心肌损害、循环和心肌局部血管紧张素Ò(AngÒ)及其受体的变化以及预先应用β受体阻断剂(B-RB)对其的影响.方法建立颅脑损伤及药物干预模型,测定血浆AngÒ水平和血清肌酸磷酸激酶同工酶(MB isoenzyme of creatine kinase,CK-MB)含量,免疫组织化学方法检测心肌AngÒ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AngÒ、心肌组织AngÒ和AT₁R水平显著升高(P<0.05).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.预先应用比索洛尔,血浆AngÒ和血清CK-MB水平比单纯损伤大鼠显著降低(P<0.05),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(RAS)可能是参与颅脑损伤后心肌损害的机制之一.B-RB具有防止颅脑损伤后心肌损害的作用.

关键词: 颅脑损伤, 心肌损害, AngÒ, AT₁R, 比索洛尔

Abstract:

Objective To investigate myocardial damage, the alterations of plasma, and myocardial angiotensin Ò and myocardial AT₁ receptor as well as the effects of bisoprolol after brain injury in rats. Methods Brain injury was induced by weight-drop technique and pretreated with bisoprolol. Plasma angiotensinÒ level was determined using RIA. Myocardial angiotensinÒand 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 Ò and serum CK-MB increased at 24 h after brain injury. AngiotensinÒ and 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 Ò and serum CK-MB decreased in bisoprolol group compared with brain injury group. Relief of myocardial damage was also observed with light and electronic microscope in bisoprolol group. Conclusion Brain injury can lead to myocardial damage. RAS maybe plays an important role in the mechanism of myocardial damage after brain injury. Bisoprolol can prevent myocardial damage after brain injury.

Key words: brain injury, myocardial damage, AngÒ, AT₁ receptor, bisoprolol

中图分类号:

Q463

郭彩霞;杜凤和;张立克;陈瑞芬;孙异临. 大鼠颅脑损伤后血管紧张素及其受体变化与B受体阻断剂对其的影响[J]. 首都医科大学学报, 2005, 26(3): 299-302.

Guo Caixia;Du Fenghe;Zhang Like;Cheng Ruifen;Sun Yilin. Myocardial Damage, Alterations of Angiotensin and Receptors after BrainInjury in Rats and Preconditional Effects of Bisoprolol on Them[J]. Journal of Capital Medical University, 2005, 26(3): 299-302.

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