Arrhythmias in rat hearts exposed to pulsed ultrasound after intravenous injection of a contrast agent

Arrhythmias in rat hearts exposed to pulsed ultrasound after intravenous injection of a contrast agent
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DOI:
10.7863/jum.2002.21.12.1347
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发表时间:
2002-12-01
影响因子:
2.3
通讯作者:
O'Brien, WD
O'Brien, WD
中科院分区:
医学4区
文献类型:
--
作者:
Zachary, JF;Hartleben, SA;O'Brien, WD

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目标。目的:建立一种适用于超声心脏注射微泡造影剂后的心电图性心律失常的动物模型。方法:研究方法。20只大鼠静脉注射造影剂0.25mL,接受脉冲超声(频率3.1 MHz;脉冲宽度13微秒;脉冲重复频率1700 Hz;原位峰值稀释压15.9 Mpa)处理,记录传导复合波和心脏病变数据。结果10只大鼠出现房性早搏、室性早搏或多形性室性心动过速。当停止超声照射时,10只大鼠中有4只停止了心律失常,但在恢复暴露时又发生了心律失常。组织化学染色(苏木精-碱性品红-苦味酸)显示16只大鼠心肌变性,但只有10只大鼠出现心律失常。心律失常大鼠心脏组织化学染色与非心律失常大鼠相比,差异无统计学意义。结论。建立了一种适合于超声辐照大鼠心脏注射微泡造影剂后的心电图心律失常的动物模型。由于心律失常主要是当造影剂与超声在暴露期间相互作用时诱发的,因此在这些极端的暴露条件下,仅有心肌变性的存在并不能充分解释异位电活动,数据表明脉冲超声通过其与造影剂的生物力学相互作用具有诱发心律失常的潜力。
Objective. To develop an animal model suitable for characterizing electrocardiographic arrhythmias in hearts exposed to ultrasound after injection of a microbubble contrast agent. Methods. Conduction complex and heart lesion data were recorded from 20 rats that received intravenous injections of 0.25 mL of a contrast agent and were exposed to pulsed ultrasound (frequency, 3.1 MHz; pulse duration, 13 microseconds; pulse repetition frequency, 1700 Hz; and in situ peak rarefactional pressure, 15,9 MPa). The volume of the contrast agent based on body weight and the mechanical index (ultrasonic pressure) exceeded those used in echocardiography by 14 to 345 and 3 to 29 times, respectively Results, Premature atrial complexes, premature ventricular complexes, or polymorphic ventricular tachycardia occurred in 10 rats. When ultrasound exposure was halted, arrhythmias ceased but reoccurred in 4 of the 10 rats when exposure resumed. Myocardial degeneration identified by histochemical staining (hematoxylin-basic fuchsin-picric acid) was observed in 16 rats; however, only 10 rats had arrhythmias. There was no significant difference in the amount of histochemical staining in hearts from rats with arrhythmias when compared with rats without arrhythmias. Conclusions. An animal model suitable for characterizing electrocardiographic arrhythmias in rat hearts exposed to ultrasound after injection of a microbubble contrast agent was developed. Because arrhythmias were induced principally when the contrast agent interacted with ultrasound during exposure, the presence of myocardial degeneration alone was not a sufficient explanation for ectopic electrical activity, Under these extreme exposure conditions, the data suggest that pulsed ultrasound through its biomechanical interactions with contrast agents has the potential to induce arrhythmias.