权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Interaction Between Electrical and Pathological Myocardial Remodeling Induced by Right and Left Ventricular Pressure Overload

右心室和左心室压力过载引起的电学和病理性心肌重塑之间的相互作用

基本信息

批准号：
15591091
负责人：
WAKIMOTO Hiroko
金额：
$ 2.24万
依托单位：
Tokyo Medical and Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2004
项目状态：
已结题

项目摘要

Propensity for proarrhythmia under the cardiac ventricular damages are considered to result from the changes of the electrical status in the heart by ventricular myocardial stretch or by other factors. This mechanism is still unknown, however, the interaction between the electrical and the pathological myocardial remodeling may play an important role in this proarrhythmia. In this study, in vivo electrophysiological studies (EPS) were performed to the monocrotaline (MCT) induced pulmonary artery hypertension model rats in order to elucidate their cardiac electrical properties and proarrhythmia. [Methods and Materials] 6weeks old male SD rats were administered MCT 0.06Omg/g (MCT) or normal saline as a control group (CTR). 4 weeks after the injection, surface ECG recordings and in vivo EPS were performed. Pentobarbital (0.033mg/g) were given into peritoneal space for the anesthesia. After 6leads-limb-ECG was recorded, 2Fr catheter with 8 polar electrodes was inserted into the heart by cut down method. The distal 4 electrodes were placed in the right ventricle while the others in the right atrium for stimulation and recording. The conventional method were used for the evaluation of electrical properties and proarrhythmia in sinus node, atrium, atrioventricular (AV) node and ventricle. [Results] The data in MCT rats (n=12) and CTR rats (n=25) were described below. sECG : SCL 162±7ms, 157±3ms, PR 45±1ms, 46±1ms, QRS 24±1ms, 35±0ms (p<0.05), corrected QT 75±6ms, 57±1ms (p<0.05). EPS : SNRT 179±4ms, 190±4ms, AVERP 78±2ms, 81±2ms, AERP 46±3ms, 22±2ms (p<0.05), Wenckebach type AV block rate by rapid atrial pacing 98±2ms, 98±1ms, 2 : 1 rate 83±2ms, 85±1ms, Wenckebach type VA block rate by rapid ventricular pacing 131±2ms, 149±5ms, RVERP 63±5ms, 42±2ms (p<0.05). Atrial tachycardia were induced in 0/12 versus 7/25 animals, whereas ventricular tachycardia in 1/12 versus 3/25.

心室损伤时致心律失常的倾向被认为是心室肌牵张或其他因素引起心脏电状态改变的结果。其机制尚不清楚，但电重构和病理性心肌重构的相互作用可能在致心律失常中起重要作用。本研究通过对野百合碱（MCT）诱导的肺动脉高压模型大鼠进行在体电生理研究（EPS），以阐明其心脏电特性和致心律失常的机制。[方法与材料] 6周龄雄性SD大鼠随机分为两组，分别给予MCT 0.060mg/g（MCT组）和生理盐水（CTR组）。注射后4周，进行体表ECG记录和体内EPS。腹腔注射戊巴比妥钠0.033mg/g。记录6导联肢体心电图后，将8极2Fr导管插入心脏。将远端4个电极放置在右心室中，而将其他电极放置在右心房中用于刺激和记录。采用常规方法评价窦房结、心房、房室结和心室的电特性和致心律失常因素。[结果] MCT大鼠（n=12）和CTR大鼠（n=25）的数据如下所述。sECG：SCL 162±7ms，157±3ms，PR 45±1ms，46±1ms，QRS 24±1ms，35±0ms（p<0.05），校正QT 75±6ms，57±1ms（p<0.05）。每股收益：SNRT 179± 4 ms，190± 4 ms，AVERP 78± 2 ms，81± 2 ms，AERP 46± 3 ms，22± 2 ms（p<0.05），快速心房起搏的文氏型房室传导阻滞率98± 2 ms，98± 1 ms，2：1频率83± 2 ms，85± 1 ms，快速心室起搏的文氏型VA传导阻滞率131± 2 ms，149± 5 ms，RVERP 63± 5 ms，42± 2 ms（p<0.05）。在0/12和7/25只动物中诱导房性心动过速，而在1/12和3/25只动物中诱导室性心动过速。