Seller R H, Banach S, Namey T, Neff M, Swartz C
Am Heart J. 1975 Apr;89(4):493-500. doi: 10.1016/0002-8703(75)90157-x.
Triamterene, amiloride, ethacrynic acid, and furosemide were studied to determine whether they modified the digitalis-induced egress of myocardial potassium which is thought to facilitate the development of digitalis arrhythmias. In a control group of 15 dogs, potassium was measured in samples obtained simultaneously from the femoral artery (FA) and the coronary sinus (CS) in a control period and at intervals after the administration of 1 mg. of acetylstrophanthidin. Acetylstrophanthidin caused a significant increase in cardiac A-V difference in the potassium concentration (CS-FA) averaging 0.47 mEq. per liter. In a group of 10 dogs, when 175 mg. of triamterene was infused prior to the acetylstrophanthidin, the rise in A-V differnece was abolished and the arrhythmias often aborted. In contrast, the infusion of potent diuretics (40 mg. of furosemide in five dogs and 100 mg. of ethacrynic acid in another five dogs) prior to acetylstrophanthidin, caused a doubling of the maximal A-V potassium difference. This study suggests that the clinical administration of antikaliuretic drugs may prevent the arrhythmias of digitalis toxicity not only by reducing kaliuresis and subsequent hypokalemia, but by a myocardial effect which antagonized the digitalis-induced loss of myocardial potassium. Contrariwise, potent diuretics may facilitate digitalis arrhythmias through a myocardial action causing a greater egress of myocardial potassium, thus explaining the development of arrhythmias despite normal serum potassium levels. These potent diuretics should be used cautiously, especially when given intravenously to patients receiving digitalis.
研究了氨苯蝶啶、阿米洛利、依他尼酸和呋塞米,以确定它们是否能改变洋地黄诱导的心肌钾外流,这种外流被认为会促进洋地黄心律失常的发生。在一个由15只狗组成的对照组中,在对照期以及给予1毫克乙酰毒毛花苷后的不同时间间隔,同时从股动脉(FA)和冠状窦(CS)采集样本测量钾含量。乙酰毒毛花苷导致心脏钾浓度的动静脉差值(CS - FA)显著增加,平均每升0.47毫当量。在一组10只狗中,在给予乙酰毒毛花苷之前输注175毫克氨苯蝶啶,动静脉差值的升高被消除,心律失常也常常中止。相反,在给予乙酰毒毛花苷之前输注强效利尿剂(5只狗输注40毫克呋塞米,另外5只狗输注100毫克依他尼酸),使最大动静脉钾差值增加了一倍。这项研究表明,抗利尿药物的临床应用可能预防洋地黄中毒引起的心律失常,不仅是通过减少尿钾排泄和随后的低钾血症,还通过一种心肌作用来对抗洋地黄诱导的心肌钾丢失。相反,强效利尿剂可能通过一种导致心肌钾外流增加的心肌作用促进洋地黄心律失常的发生,从而解释了尽管血清钾水平正常仍会出现心律失常的原因。这些强效利尿剂应谨慎使用,尤其是静脉给予接受洋地黄治疗的患者时。