Goldenberg I F, Olivari M T, Levine T B, Cohn J N
Minneapolis Heart Institute Foundation, Minnesota 55407.
Am J Cardiol. 1989 Apr 1;63(12):843-6. doi: 10.1016/0002-9149(89)90054-4.
Dobutamine was administered in a dose of 10 +/- 1 micrograms/kg/min to 13 patients with severe idiopathic or ischemic dilated cardiomyopathy. Acute hemodynamic improvement was noted in all patients. All patients had a significant decrease in plasma potassium (4.6 +/- 0.1 to 4.2 +/- 0.2 mEq/liter, p less than 0.0001) at peak infusion. The decrease in potassium persisted for at least 45 minutes after discontinuing the infusion. Three patients had exacerbation of baseline ventricular arrhythmias that resolved with infusion discontinuation. Changes in plasma norepinephrine could not explain the potassium decrease or arrhythmia production, which also significantly decreased in these patients (771 +/- 123 to 524 +/- 73 pg/ml, p less than 0.01). It is concluded that dobutamine causes a significant decrease in plasma potassium and that the decrease persists at least 45 minutes after the infusion is discontinued.
对13例重症特发性或缺血性扩张型心肌病患者给予剂量为10±1微克/千克/分钟的多巴酚丁胺。所有患者均出现急性血流动力学改善。所有患者在输注高峰时血浆钾显著降低（从4.6±0.1降至4.2±0.2毫当量/升，p<0.0001）。输注停止后，钾的降低持续至少45分钟。3例患者基线室性心律失常加重，停止输注后缓解。血浆去甲肾上腺素的变化无法解释钾的降低或心律失常的产生，这些患者的血浆去甲肾上腺素也显著降低（从771±123降至524±73皮克/毫升，p<0.01）。结论是多巴酚丁胺可导致血浆钾显著降低，且在输注停止后至少45分钟内这种降低持续存在。
