Light G S, Hellyer P W
Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh 27601.
Am J Vet Res. 1993 Dec;54(12):2099-103.
We investigated the influence of parasympathetic tone on the arrhythmogenic dose of dobutamine in horses premedicated with xylazine, anesthetized with guaifenesin and thiamylal, and maintained on halothane in oxygen. Six horses were used in 12 randomized trials. In each trial, after end-tidal halothane concentration was stabilized at 1.1% (1.25 times minimum alveolar concentration [MAC]) in oxygen, either saline solution (0.02 ml/kg of body weight) or atropine (0.04 mg/kg) was administered IV. Five minutes later, dobutamine infusion was started at dosage of 2.5 micrograms/kg/min, IV. The dobutamine infusion was continued for 10 minutes, or until 4 or more premature ventricular complexes occurred within 15 seconds, or sustained narrow-complex tachyarrhythmia clearly not sinus in nature occurred. If the criteria for termination were not met, dobutamine infusion was increased by 2.5 micrograms/kg/min, after the hemodynamic variables had returned to baseline. The horses were allowed to recover, and were rested for at least 1 week before the second trial. The arrhythmogenic dose of dobutamine was calculated by multiplying the infusion rate by the elapsed time into infusion when arrhythmia occurred. There was significant difference between the arrhythmogenic dose of dobutamine (ADD) in saline-treated horses (mean +/- SEM, ADD = 105.6 +/- 16.3 micrograms/kg) and atropinized horses (ADD = 36.2 +/- 8.7 micrograms/kg). There were no differences in the prearrhythmia or immediate postarrhythmia ventricular heart rate (HR) or systolic (SAP), diastolic (DAP), or mean (MAP) arterial pressures between treated and control groups. The change in hemodynamic variables from prearrhythmia to immediate postarrhythmia formation was not different between the 2 groups. (ABSTRACT TRUNCATED AT 250 WORDS)
我们研究了副交感神经张力对用赛拉嗪进行术前用药、用愈创甘油醚和硫喷妥钠麻醉并在氧气中维持氟烷麻醉的马匹中多巴酚丁胺致心律失常剂量的影响。在12项随机试验中使用了6匹马。在每项试验中,当呼气末氟烷浓度在氧气中稳定在1.1%(1.25倍最低肺泡浓度[MAC])后,静脉注射生理盐水(0.02 ml/kg体重)或阿托品(0.04 mg/kg)。5分钟后,开始以2.5微克/千克/分钟的剂量静脉输注多巴酚丁胺。多巴酚丁胺输注持续10分钟,或直至15秒内出现4次或更多室性早搏,或出现明显非窦性的持续性窄QRS波心动过速。如果未达到终止标准,在血流动力学变量恢复到基线后,多巴酚丁胺输注速率增加2.5微克/千克/分钟。马匹恢复后,在第二次试验前休息至少1周。多巴酚丁胺的致心律失常剂量通过将输注速率乘以心律失常发生时的输注时间来计算。生理盐水处理组马匹(平均值±标准误,致心律失常剂量[ADD]=105.6±16.3微克/千克)和阿托品处理组马匹(ADD=36.2±8.7微克/千克)的多巴酚丁胺致心律失常剂量之间存在显著差异。治疗组和对照组在心律失常前或心律失常后即刻的心室心率(HR)或收缩压(SAP)、舒张压(DAP)或平均动脉压(MAP)方面没有差异。两组从心律失常前到心律失常即刻形成时血流动力学变量的变化没有差异。(摘要截断于250字)