Neustein S M, Dimich I, Sampson I, Sadeghi A, Mezrow C, Shiang H
Department of Anesthesiology, Mount Sinai School of Medicine, of the City University of New York, NY.
Can J Anaesth. 1994 Jun;41(6):542-6. doi: 10.1007/BF03011552.
Dopexamine hydrochloride (Dopacard) is the novel synthetic catecholamine designed for use in the acute management of a low cardiac output status. In addition to dopaminergic receptor stimulation, dopexamine hydrochloride is a potent beta 2 adrenoceptor agonist with negligible direct beta 1 and no alpha adrenergic effect. The objective of this study was to compare the arrhythmogenic effects of dopexamine hydrochloride and dopamine in dogs anaesthetized with halothane (1.2 MAC). The starting dose for dopexamine hydrochloride was 3.5 micrograms.kg-1.min-1 and for dopamine was 5 micrograms.kg-1.min-1. Concentrations of the drugs were increased until four or more premature ventricular contractions within 15 seconds were produced. All dogs developed ventricular tachycardia when dopamine was administered in concentrations ranging between 18-20 micrograms.kg-1.min-1. Unlike dopamine, dopexamine hydrochloride even at concentrations as high as 50 micrograms.kg-1.min-1 did not induce any atrial or ventricular ectopic beats. Lack of beta 1 and alpha adrenergic agonist effects is a likely explanation for low arrhythmogenicity of dopexamine hydrochloride. Both drugs increase cardiac output; dopexamine hydrochloride primarily by a dose-related increase in heart rate and increased afterload. At the maximal concentration dopexamine hydrochloride increased heart rate from 114 to 150 beat.min-1, mean arterial pressure decreased from 81 mmHg to 45 mmHg and SVR decreased from 2418 to 962 dyne.sec-1cm-5. Myocardial contractility increased only moderately, as evaluated by dP/dt, which increased from 1290 to 1696 mmHg.sec-1. Dopamine had a more marked inotropic effect: the dP/dt increased, at the maximal concentration, from 1480 to 2570 mmHg.sec-1.(ABSTRACT TRUNCATED AT 250 WORDS)
盐酸多培沙明（多帕卡德）是一种新型合成儿茶酚胺，用于急性处理低心排血量状态。除刺激多巴胺能受体外，盐酸多培沙明还是一种强效β2肾上腺素能受体激动剂，对β1受体的直接作用可忽略不计，且无α肾上腺素能效应。本研究的目的是比较盐酸多培沙明和多巴胺对用氟烷（1.2MAC）麻醉的犬的致心律失常作用。盐酸多培沙明的起始剂量为3.5微克·千克-1·分钟-1，多巴胺的起始剂量为5微克·千克-1·分钟-1。药物浓度逐渐增加，直至15秒内出现4次或更多室性早搏。当多巴胺以18 - 20微克·千克-1·分钟-1的浓度给药时，所有犬均发生室性心动过速。与多巴胺不同，即使盐酸多培沙明浓度高达50微克·千克-1·分钟-1，也未诱发任何房性或室性异位搏动。缺乏β1和α肾上腺素能激动剂效应可能是盐酸多培沙明致心律失常性低的原因。两种药物均增加心排血量；盐酸多培沙明主要通过与剂量相关的心率增加和后负荷增加来实现。在最大浓度时，盐酸多培沙明使心率从114次/分钟增加到150次/分钟，平均动脉压从81mmHg降至45mmHg，全身血管阻力从2418降至962达因·秒-1·厘米-5。通过dp/dt评估，心肌收缩力仅适度增加，从1290mmHg·秒-1增加到1696mmHg·秒-1。多巴胺具有更显著的正性肌力作用：在最大浓度时，dp/dt从1480mmHg·秒-1增加到2570mmHg·秒-1。（摘要截短于250字）
