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通过超声心动图和血流动力学方法评估犬尖端扭转型室性心动过速模型的心血管特征。

Cardiovascular profile of the canine torsades de pointes arrhythmia model assessed by echocardiographic and haemodynamic methods.

作者信息

Takahara Akira, Sugiyama Atsushi, Satoh Yoshioki, Iwasaki Hiroshi, Nakamura Yuji, Hashimoto Keitaro

机构信息

Department of Pharmacology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Yamanashi, Japan.

出版信息

Basic Clin Pharmacol Toxicol. 2007 Jul;101(1):35-40. doi: 10.1111/j.1742-7843.2007.00071.x.

DOI:10.1111/j.1742-7843.2007.00071.x
PMID:17577314
Abstract

Chronic atrioventricular block dogs have been established as an in vivo model of drug-induced torsades de pointes arrhythmias. We compared the cardiovascular profile of the canine model with that of sham-operated animals using echocardiographic and haemodynamic methods. In the echocardiographic study, the larger diameters of the left atria, inferior vena cava and left ventricle in end-diastole in addition to greater fractional shortening, end-diastolic volume, stroke volume and ejection fraction were more often detected in the chronic atrioventricular block dogs than in the sham-operated animals. During haemodynamic examination, lower cardiac output and higher pulmonary capillary wedge pressure were detected in chronic atrioventricular block dogs more than in sham-operated animals; however, these changes were within the physiological limits, and the results suggest that the chronic atrioventricular block dogs have a pathophysiological profile of chronic compensated heart failure.

摘要

慢性房室传导阻滞犬已被确立为药物诱导的尖端扭转型室性心律失常的体内模型。我们使用超声心动图和血流动力学方法,将犬模型的心血管特征与假手术动物的进行了比较。在超声心动图研究中,与假手术动物相比,慢性房室传导阻滞犬更常检测到舒张末期左心房、下腔静脉和左心室的直径更大,以及更大的缩短分数、舒张末期容积、每搏输出量和射血分数。在血流动力学检查中,慢性房室传导阻滞犬比假手术动物更常检测到心输出量降低和肺毛细血管楔压升高;然而,这些变化在生理范围内,结果表明慢性房室传导阻滞犬具有慢性代偿性心力衰竭的病理生理特征。

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Cardiovascular profile of the canine torsades de pointes arrhythmia model assessed by echocardiographic and haemodynamic methods.通过超声心动图和血流动力学方法评估犬尖端扭转型室性心动过速模型的心血管特征。
Basic Clin Pharmacol Toxicol. 2007 Jul;101(1):35-40. doi: 10.1111/j.1742-7843.2007.00071.x.
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[Torsade de pointes--a cause of Morgagni-Adam-Stokes attacks in patients with complete atrioventricular block].[尖端扭转型室速——完全性房室传导阻滞患者莫加尼-亚当-斯托克斯发作的一个原因]
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引用本文的文献

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Front Pharmacol. 2023 Jan 19;14:1055031. doi: 10.3389/fphar.2023.1055031. eCollection 2023.
2
Long-term blockade of L/N-type Ca(2+) channels by cilnidipine ameliorates repolarization abnormality of the canine hypertrophied heart.西尼地平通过阻断 L/N 型钙通道改善犬肥厚心脏复极化异常。
Br J Pharmacol. 2009 Nov;158(5):1366-74. doi: 10.1111/j.1476-5381.2009.00407.x. Epub 2009 Sep 28.
3
Sensitive and reliable proarrhythmia in vivo animal models for predicting drug-induced torsades de pointes in patients with remodelled hearts.
用于预测心脏重构患者药物诱导尖端扭转型室速的敏感且可靠的体内致心律失常动物模型。
Br J Pharmacol. 2008 Aug;154(7):1528-37. doi: 10.1038/bjp.2008.240. Epub 2008 Jun 16.