急性血栓阻塞性冠状动脉缺血模型及其心律失常机制(摘要)
作者：张澍
单位：北京市，中国医学科学院 中国协和医科大学 心血管病研究所 阜外心血管病医院 临床电生理研究室(100037)
关键词：
目的 目的：急性心肌缺血所致自发性VT的发生率因实验模型差别和多种影响因素存在而不同。室性心动速的发生率在血栓性阻塞的模型较非血栓性阻塞的高。本人研究急性血栓阻塞情况下自发性VT的发生及其心律失常机理。
方法：应用微小阳极电流(200～300微安)刺激冠状动脉左旋支(LCX)近端内膜，在10只麻醉开胸狗进行了诱发血栓观察自发性VT的发生并以三维标测技术研究心律失常机制。
结果：释放致栓电流诱发LCX完全阻塞需35～60(平均47±18)分。引起LCX完全阻塞所需要的电流为200～300(平均255)微安。在血栓形成过程中所有动物均见室性早搏，9/10动物发生非持续性心动过速(NSVT)，开始于LCX完全阻塞的前5分，其发生大多由于局灶性机制并且起源于多个不同部位。LCX完全阻塞后有6只动物诱发出持续性室速(SusVT),其中4例为Ⅰa型，2例为Ⅰb。Ⅰa型SusVT发生在LCX完全阻塞后3～7分且在SusVT后10～41秒蜕变为VF。Ⅰb型SusVT发生在LCX完全阻塞后13～22分，SusVT均能自行终止其中1例于14分后发生4个连续室性早搏转而VF。SusVT的诱发均由于局灶性机制，其中4例起源于缺血边缘区域，2例在缺血区。SusVT维持在3/6例是由于缺血边缘区局灶性机制，另3例是由于心肌内的一个大折返路径，即以前壁缺血区心内膜下经间隔作为快径，而左心室后壁心外膜并经心肌内返回心内膜下作为慢径，而VF是由于多发的折返波形成。
, 百拇医药
结论：向血管内膜释放微小的阳性电以刺激局部血栓形成的可作为一种较为可靠的实验动物模型用来研究心肌缺血的病理生理学改变。
An Animal Model of Thrombotic Occlusion of Coronary Artery and Ventricular Arrhythmias(Abstract)
Department of Clinical Electrophysiology, Cardiovascular Institute and Fu Wai Hospital, CAMS and PUMC, Beijing (100037)
Zhang Shu.
Objective: To further identify the occurrence and mechanism of spontaneous ventricular tachycardia caused by thrombotic coronary occlusion.
, 百拇医药
Methods: Regional ischemia was induced by thrombotic occlusion using a wire electrode to deliver a 200～300 μA anodic current to the intima of the proximal left circumflex artery (LCX) in 10 open-chest dogs.
Results: Total occlusion occurred 47±18 minutes after delivery of the current as indicated by a Doppler flowmeter. Current required to totalk occlusion of LCX was 200～300 (mean 255)μA. In nine dogs, nonsustained VT (NSVT) originated from numerous, different focal sites was initiated and maintained. Sustained VT (susVT) occurred in six dogs and was also initiated by focal mechanisms located near the ischemic border in four dogs and within the ischemic region in the other two. In three dogs, the susVT was maintained primarily through a focal mechanism, which arose in the ischemic border region. In the other three dogs, susVT was maintained by macroreentry extended from the subendocardium of the ischemic region anteriorly through the septum as the fast pathway, towards the epicardium of the posterior area of LV and then intramurally back to the subendocardium as the slow pathway. VT changed into VF within 10～41 seconds in four of these six dogs. The transition from VT to VF was due exclusively to intramural reentry with multiple wavefronts involving the nonischemic region in three dogs, the ischemic border region in one, and the ischemic region in one.
Conclusion: Thrombotic occlusion of coronary artery by delivering anodic current to intima of the vessel is a useful model to study the pathophysiological mechanism of acute ischemia., 百拇医药
单位：北京市，中国医学科学院 中国协和医科大学 心血管病研究所 阜外心血管病医院 临床电生理研究室(100037)
关键词：
目的 目的：急性心肌缺血所致自发性VT的发生率因实验模型差别和多种影响因素存在而不同。室性心动速的发生率在血栓性阻塞的模型较非血栓性阻塞的高。本人研究急性血栓阻塞情况下自发性VT的发生及其心律失常机理。
方法：应用微小阳极电流(200～300微安)刺激冠状动脉左旋支(LCX)近端内膜，在10只麻醉开胸狗进行了诱发血栓观察自发性VT的发生并以三维标测技术研究心律失常机制。
结果：释放致栓电流诱发LCX完全阻塞需35～60(平均47±18)分。引起LCX完全阻塞所需要的电流为200～300(平均255)微安。在血栓形成过程中所有动物均见室性早搏，9/10动物发生非持续性心动过速(NSVT)，开始于LCX完全阻塞的前5分，其发生大多由于局灶性机制并且起源于多个不同部位。LCX完全阻塞后有6只动物诱发出持续性室速(SusVT),其中4例为Ⅰa型，2例为Ⅰb。Ⅰa型SusVT发生在LCX完全阻塞后3～7分且在SusVT后10～41秒蜕变为VF。Ⅰb型SusVT发生在LCX完全阻塞后13～22分，SusVT均能自行终止其中1例于14分后发生4个连续室性早搏转而VF。SusVT的诱发均由于局灶性机制，其中4例起源于缺血边缘区域，2例在缺血区。SusVT维持在3/6例是由于缺血边缘区局灶性机制，另3例是由于心肌内的一个大折返路径，即以前壁缺血区心内膜下经间隔作为快径，而左心室后壁心外膜并经心肌内返回心内膜下作为慢径，而VF是由于多发的折返波形成。
, 百拇医药
结论：向血管内膜释放微小的阳性电以刺激局部血栓形成的可作为一种较为可靠的实验动物模型用来研究心肌缺血的病理生理学改变。
An Animal Model of Thrombotic Occlusion of Coronary Artery and Ventricular Arrhythmias(Abstract)
Department of Clinical Electrophysiology, Cardiovascular Institute and Fu Wai Hospital, CAMS and PUMC, Beijing (100037)
Zhang Shu.
Objective: To further identify the occurrence and mechanism of spontaneous ventricular tachycardia caused by thrombotic coronary occlusion.
, 百拇医药
Methods: Regional ischemia was induced by thrombotic occlusion using a wire electrode to deliver a 200～300 μA anodic current to the intima of the proximal left circumflex artery (LCX) in 10 open-chest dogs.
Results: Total occlusion occurred 47±18 minutes after delivery of the current as indicated by a Doppler flowmeter. Current required to totalk occlusion of LCX was 200～300 (mean 255)μA. In nine dogs, nonsustained VT (NSVT) originated from numerous, different focal sites was initiated and maintained. Sustained VT (susVT) occurred in six dogs and was also initiated by focal mechanisms located near the ischemic border in four dogs and within the ischemic region in the other two. In three dogs, the susVT was maintained primarily through a focal mechanism, which arose in the ischemic border region. In the other three dogs, susVT was maintained by macroreentry extended from the subendocardium of the ischemic region anteriorly through the septum as the fast pathway, towards the epicardium of the posterior area of LV and then intramurally back to the subendocardium as the slow pathway. VT changed into VF within 10～41 seconds in four of these six dogs. The transition from VT to VF was due exclusively to intramural reentry with multiple wavefronts involving the nonischemic region in three dogs, the ischemic border region in one, and the ischemic region in one.
Conclusion: Thrombotic occlusion of coronary artery by delivering anodic current to intima of the vessel is a useful model to study the pathophysiological mechanism of acute ischemia., 百拇医药