Akita M, Kuwahara M, Tsubone H, Sugano S
Department of Comparative Pathophysiology, Graduate School of Agriculture and Life Sciences, University of Tokyo, Japan.
J Electrocardiol. 1998 Jan;31(1):45-9. doi: 10.1016/s0022-0736(98)90006-1.
Electrolyte abnormalities have become an increasingly important cause of arrhythmias owing to the widespread use of high-potency diuretics. Hypokalemia is one of the common complications of diuretic use. Although some studies of hypokalemia induced by furosemide as well as of potassium-deficient diets in the rat have been reported, the electrocardiographic (ECG) changes during hypokalemia in the rat are poorly understood. This study was designed to examine such changes. For this purpose, hypokalemia was induced by furosemide administration, and the diagnostic criteria for ECG manifestations of hypokalemia were determined. During hypokalemia, conduction in most parts of the heart was suppressed to an extent depending on plasma potassium concentration. Prolongation of the QT interval was also observed, which agrees with findings in humans and dogs. Furthermore, prolonged durations of the P wave and QRS complex were observed during hypokalemia in the rat. The extent of alteration of the PR interval induced by hypokalemia was less significant than that of P wave and QRS complex durations. These results suggest that the excitabilities of the myocardium in the atria and ventricles may be affected by extracellular potassium level rather than by the atrioventricular conduction system in the rat. Wave amplitude, except that of the P wave, was decreased by severe hypokalemia. These changes were not dependent on the plasma potassium concentration. Typical T wave changes observed with hypokalemia in humans and dogs did not occur in the rat. The ECG manifestations of acute hypokalemia in the rat did not include the typical T wave changes seen in species with ST-segment type ECGs; however, other ECG parameter changes occurring with hypokalemia were qualitatively similar to those in other species. These results may be useful for testing the toxicity of potassium-depleting drugs in the rat.
由于高效利尿剂的广泛使用,电解质异常已成为心律失常日益重要的原因。低钾血症是使用利尿剂的常见并发症之一。尽管已有一些关于速尿诱导大鼠低钾血症以及低钾饮食的研究报道,但对大鼠低钾血症期间的心电图(ECG)变化了解甚少。本研究旨在检查此类变化。为此,通过给予速尿诱导低钾血症,并确定低钾血症心电图表现的诊断标准。在低钾血症期间,心脏大部分区域的传导受到抑制,其程度取决于血浆钾浓度。还观察到QT间期延长,这与人类和犬类的研究结果一致。此外,在大鼠低钾血症期间观察到P波和QRS波群时限延长。低钾血症引起的PR间期改变程度不如P波和QRS波群时限改变明显。这些结果表明,在大鼠中,心房和心室心肌的兴奋性可能受细胞外钾水平影响,而非受房室传导系统影响。除P波外,严重低钾血症会使波幅降低。这些变化与血浆钾浓度无关。在人类和犬类中观察到的低钾血症典型T波改变在大鼠中未出现。大鼠急性低钾血症的心电图表现不包括具有ST段型心电图的物种中所见的典型T波改变;然而,低钾血症时发生的其他心电图参数变化在性质上与其他物种相似。这些结果可能有助于测试大鼠中排钾药物的毒性。