盐酸多西普兰加重肾上腺素引起的心律失常并伴有双向室性心动过速。

ISRN cardiology Pub Date : 2014-01-09 eCollection Date: 2014-01-01 DOI:10.1155/2014/212045
Shota Oikawa, Hiroko Nomura, Miki Nishio, Rina Nagata, Tadayoshi Hata
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引用次数: 1

摘要

目标。盐酸多西普兰是一种呼吸兴奋剂,对心肌IK1钾通道有抑制作用,被认为增加心肌细胞的膜不稳定性和兴奋性。我们在氟烷肾上腺素致心律失常大鼠模型中观察盐酸多西普兰的致心律失常作用。方法。实验选用12-14周龄Wistar雌性大鼠13只。用吸入氟烷麻醉动物,观察盐酸多西普兰对氟烷肾上腺素引起的心律失常的影响。研究心电图复极特征(QT、QTc、JTp、JT和Tp-e间期)的时间依赖性变化。结果。盐酸多西普兰本身不诱发心律失常,但肾上腺素加入后可诱发双向室性心动过速。结论。在肌浆网蛋白没有遗传异常的情况下,药物诱导的细胞内Ca(2+)调节损伤导致BVT。
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Doxapram hydrochloride aggravates adrenaline-induced arrhythmias accompanied by bidirectional ventricular tachycardia.

Objectives. Doxapram hydrochloride is a respiratory stimulant that has an inhibitory effect on myocardial IK1 potassium channels and is thought to increase membrane instability and excitability in myocardial cells. We examined the arrhythmogenic effects of doxapram hydrochloride in a rat model of halothane adrenaline-induced arrhythmia. Methods. Thirteen female Wistar rats (12-14 weeks old) were used in the study. Animals were anesthetized with inhalation of halothane to permit observation of the effects of doxapram hydrochloride on halothane adrenaline-induced arrhythmia. Time-dependent changes in ECG repolarization characteristics (QT, QTc, JTp, JT, and Tp-e intervals) were studied. Results. Doxapram hydrochloride itself did not induce arrhythmia but did induce bidirectional ventricular tachycardia after addition of adrenaline. Conclusion. Drug-induced impairment of intracellular Ca(2+) regulation caused BVT in the absence of genetic abnormalities in proteins in the sarcoplasmic reticulum.

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