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沙丁胺醇诱发清醒犬低钾血症的心脏效应

Cardiac effects of salbutamol-induced hypokalaemia in the conscious dog.

作者信息

Wahlqvist M L, Shanahan E A, Dennis P M, Pullan P T, Wilmshurst E G

出版信息

Clin Exp Pharmacol Physiol. 1978 Nov-Dec;5(6):617-25. doi: 10.1111/j.1440-1681.1978.tb00717.x.

Abstract
  1. Infusion of salbutamol (3.0 microgram/min after a bolus injection of 100 microgram) produced hypokalaemia in conscious dogs. 2. Measurement of arterial and coronary sinus potassium differences revealed no significant potassium loss from the heart with established hypokalaemia. 3. Shortly after the initial salbutamol bolus and before steady-state hypokalaemia had been achieved during salbutamol infusion, a prolongation of QTc occurred; this corresponded to a significant myocardial potassium of -0.12 mmol/l plasma. 4. Urinary electrolyte excretions indicated that the hypokalaemia was not due to urinary potassium loss. 5. It was deduced that potassium had moved intracellularly. No change in hydrogen ion status occurred to account for this. Pronounced rises in plasma insulin immunoreactivities during salbutamol infusions suggested this as one mechanism for potassium shifts.
摘要
  1. 给清醒犬静脉注射沙丁胺醇100微克后,以3.0微克/分钟的速度输注,可导致低钾血症。2. 测量动脉血和冠状窦的钾差异,结果显示在已形成低钾血症的情况下,心脏无明显钾流失。3. 在首次静脉注射沙丁胺醇后不久,且在输注沙丁胺醇期间尚未达到稳态低钾血症之前,QTc间期延长;这与血浆心肌钾显著降低0.12 mmol/l相对应。4. 尿电解质排泄表明,低钾血症并非由尿钾流失所致。5. 由此推断钾已移入细胞内。氢离子状态未发生变化以解释这一现象。沙丁胺醇输注期间血浆胰岛素免疫反应性显著升高,提示这是钾转移的一种机制。

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