BACKGROUND: Craniocerebral injury can cause a series of visceral complications, among which cardiovascular complication is paid special attention.OBJECTIVE: To investigate the effects of craniocerebral injury on changes of circulatory and local angiotensin Ⅱ (Ang Ⅱ ) and local angiotensin Ⅱ receptor 1 (AT1) in the heart.DESIGN: Randomized controlled experiment taking animals as subjects.SETTING: Beijing Tiantan Hospital, and the College of Basic Medicine,Capital University of Medical Sciences.MATERIALS: The experiment was conducted at the Central Laboratory of Capital University of Medical Sciences and the Central Laboratory of Beijing Tiantan Hospital from 2003 to 2004. Totally 40 healthy male Wistar rats were divided randomly into craniocerebral injury group and control group with 20 in each group.METHODS: Rats in craniocerebral injury group were treated with weightdrop method to establish the model of craniocerebral injury, while rats in control group received no impact. Twenty-four hours after hitting, 10 rats in each group were selected to assay their Ang Ⅱ and AT1; the other 10 in each group were selected to observe their myocardial forms.myocardium of rats assayed with light microscope after hematoxylin-eosin staining and transmission electron microscope.It was significantly higher in craniocerebral injury group than in control ity: It was obviously higher in craniocerebral injury group than in control Ⅱ and AT1: The area of positive reactant and gray value in craniocerebral toxylin-eosin staining: Strong acidophil staining was found on myocardial cellular plasma in craniocerebral injury group. The results showed that cytoplasm shrank obviously; muscle fiber broke, decreased or disappeared.Focal hydropic degeneration, lysis or necrosis was observed in myocardium.Ultrastructural pathological observation revealed pathological damage of myocardium.CONCLUSION: Craniocerebral injury in rats can cause myocardial damage, and changes of angiotensin system may be one of the factors.%背景:颅脑损伤可以引起一系列的内脏并发症,其中心血管并发症日益引起人们的重视.目的:探讨颅脑损伤所致循环和心脏局部血管紧张素Ⅱ及心脏局部血管紧张素Ⅱ1型受体水平的变化.设计:随机对照动物实验.单位:首都医科大学附属北京天坛医院和首都医科大学基础医学院.材料:实验于2003/2004在首都医科大学中心实验室和北京天坛医院中心实验室进行.健康雌性Wistar大鼠40只,随机分为颅脑损伤组和对照组两组,每组20只.方法:颅脑损伤组用局部重物撞击法建立大鼠颅脑损伤模型,对照组不打击.在撞击即时点后24 h取材,每组10只用于血管紧张素Ⅱ及其1型受体检测,另外10只用于心肌病例形态观察.主要观察指标:①用均相竞争放免法测定血浆血管紧张素Ⅱ水平.②采用免疫组织化学方法检测心肌血管紧张素Ⅱ及其1型受体的表达.③采用酶反应速率法测定血清肌酸磷酸激酶同工酶活性.④苏木精-伊红染色,光镜,透射电镜观察大鼠心肌超微结构等病理形态学改变.结果:40只大鼠进入结果分析.①血浆血管紧张素Ⅱ水平:颅脑损伤组明显高于对照组[(965.52±176.71),(485.03±86.13)ng/L,P＜0.05].②血清肌酸磷酸激酶同工酶活性:颅脑损伤组显著高于对照组[(12.77±4.07),(3.49±1.55)μkat/L,P＜0.05].③心肌血管紧张素Ⅱ及其1型受体的表达:颅脑损伤组的阳性反应物面积与灰度值均高于对照组(P＜0.05).④苏木精-伊红染色颅脑损伤组心肌细胞胞浆强嗜酸性染色,明显的胞质皱缩,肌纤维断裂、减少或消失,可见心肌局灶性水样变性、溶解或坏死.超微结构的病理观察均见心肌病理损害.结论:大鼠颅脑损伤可导致心肌损害的发生,血管紧张素系统变化可能是其因素之一.
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