Zachary James F, Hartleben Sarah A, Frizzell Leon A, O'Brien William D
Bioengineering Program, University of Illinois at Urbana-Champaign, 61802, USA.
J Ultrasound Med. 2002 Dec;21(12):1347-56; discussion 1343-45. doi: 10.7863/jum.2002.21.12.1347.
To develop an animal model suitable for characterizing electrocardiographic arrhythmias in hearts exposed to ultrasound after injection of a microbubble contrast agent.
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, 1.3 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.
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 fuchsinpicric 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.
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.
建立一种动物模型，用于表征注射微泡造影剂后暴露于超声的心脏中的心电图心律失常。
记录20只大鼠的传导复合体和心脏病变数据，这些大鼠静脉注射0.25 mL造影剂并暴露于脉冲超声（频率3.1 MHz；脉冲持续时间1.3微秒；脉冲重复频率1700 Hz；原位峰值稀疏压力15.9 MPa）。基于体重的造影剂体积和机械指数（超声压力）分别比超声心动图中使用的超出14至345倍和3至29倍。
10只大鼠出现房性早搏、室性早搏或多形性室性心动过速。当停止超声暴露时，心律失常停止，但在10只大鼠中有4只在恢复暴露时再次出现。通过组织化学染色（苏木精-碱性品红苦味酸）鉴定的心肌变性在16只大鼠中观察到；然而，只有10只大鼠有心律失常。与没有心律失常的大鼠相比，有心律失常的大鼠心脏中的组织化学染色量没有显著差异。
建立了一种适用于表征注射微泡造影剂后暴露于超声的大鼠心脏中心电图心律失常的动物模型。因为心律失常主要是在暴露期间造影剂与超声相互作用时诱发的，所以仅心肌变性的存在不足以解释异位电活动。在这些极端暴露条件下，数据表明脉冲超声通过其与造影剂的生物力学相互作用有可能诱发心律失常。
