首都医科大学学报 ›› 2008, Vol. 29 ›› Issue (3): 300-304.

• 基础研究 • 上一篇    下一篇

急性脑损伤致心肌损害及内源性5-羟色胺改变

郭彩霞1, 杜凤和1, 张立克2, 芦玲巧2, 陈瑞芬3, 孙异临4   

  1. 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病理生理学教研室;3. 首都医科大学基础医学院病理解剖学教研室;4. 首都医科大学附属北京天坛医院电镜室
  • 收稿日期:2007-01-11 修回日期:1900-01-01 出版日期:2008-06-24 发布日期:2008-06-24
  • 通讯作者: 杜凤和

Myocardial Damages and Alterations of 5-HT after Acute Brain Injury in Rats

Guo Caixia1, Du Fenghe1, Zhang Like2, Lu Lingqiao2, Chen Ruifen3, Sun Yilin4   

  1. 1. Department of Cardiovascular Medicine, Beijing Tiantan Hospital, Capital Medical University;2. Department of Pathophysiology, School of Basic Medical Sciences, Capital Medical University;3. Department of Pathology, School of Basic Medical Sciences, Capital Medical University;4. Department of Electron Microscopy, Beijing Tiantan Hospital, Capital Medical University
  • Received:2007-01-11 Revised:1900-01-01 Online:2008-06-24 Published:2008-06-24

摘要: 目的 探讨急性脑损伤所致心肌损害的表现和内源性5-HT的变化规律,为了解急性脑损伤所致心肌损害的特点和发生机制提供理论依据.方法 采用急性脑损伤动物模型观察心电、心功能、肌酸激酶同工酶(CK-MB)含量、心肌HE染色及超微结构改变判断心肌损害与否及损伤程度,采用高效液相色谱-电化学检测(HPLC-ECD)测定血浆及心肌组织5-羟色胺(5-HT)水平,观察1、6、24和48h时间点的变化.结果 急性脑损伤致心肌损害表现为心电异常增多(P<0.05);心室收缩舒张功能减低,包括左心室内压上升/下降最大变化率(±dp/dtmax)和左心室发展压(LVDP)显著下降(P<0.05),左心室舒张末压(LVEDP)升高(P<0.05);CK-MB含量增加(P<0.05);HE染色和超微结构可见心肌灶状变性、坏死及出血等.急性脑损伤后24h心肌损害最严重.血浆5-HT水平升高(P<0.05).血浆5-HT水平与CK-MB含量呈正相关(P<0.05).结论 急性脑损伤可以导致心肌损害的发生,使内源性5-HT的产生增加,5-HT可能参与急性脑损伤后的心肌损害.

关键词: 急性脑损伤, 心肌损害, 5-HT

Abstract: Objective More and more researchers become focused on myocardial damages after acute brain injury are diverse.Characteristics of myocardial damages after acute brain injury are divere.The mechanism is not clear and there isn't affirmative method of prevention and treatment.It is of important clinical significance to study the mechanism,prevention and treatment to improve prognosis,decrease mortality and increase the number of heart donation.Objectives of this study are to investigate the process of myocardial damage after acute brain injury and to study the effects of 5-HT in plasma and myocardium on myocardial damage after acute brain injury in rat.The study can provide further insights into the relationship between the brain and the heart,and the prevention and treatment of myocardial injury after acute brain injury.Methods Acute brain injury rat model was induced with weight-drop technique.Electrocardiogram,cardiac function,serum CK-MB(heart-type creatine kinase isoenzyme) and morphologic alterations in myocardium were measured to indicate and diagnose the degree of myocardial damage.Electrocardiogram was recorded using twelve leads electro cardiograph.Alterations of cardiac function included ±dp/dtmax,LVDP(left ventricular developed pressure) and LVEDP(left ventricular diastolic end pressure).serum CK-MB was measured using enzyme reaction rate method.The morphologic alterations in myocardium were observed with light and electronic microscopes.5-HT in plasma and myocardium were detected by high performance liquid chromatography-electrical conductivity detector.Rats were divided into sham group and acute brain injury group in the experiment.Alterations were observed at 4 time point including 1 hour,6 hour,24 hour and 48 hour after acute brain injury.Results The cardiac abnormalities after acute brain injury had been shown as below.Incidence of abnormal ECG increased(P<0.05);Positive and negative dp/dtmax and LVDP decreased(P<0.05);LVEDP increased(P<0.05);CK-MB increased(P<0.05).Degeneration,necrosis and hemorrhage of myocardium were observed by light and electronic microscopes,which included increasing and swelling of mitochondria and disruption of cardiac muscle fiber.The most severe myocardial damage happened in 24 hours after ABI.Myocardial systolic dysfunction happened earlier than diastolic dysfunction.Plasma 5-HT increased significantly(P<0.05).Positive correlation was found between 5-HT in plasma and CK-MB(P<0.05).Conclusion Acute brain injury can lead to myocardial damage.5-HT may play an important role in the mechanism of myocardial damage after brain injury.

Key words: acute brain injury, myocardial damage, 5-HT

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