Korean Circ J.
1971 Jun;1(1):1-22. 10.4070/kcj.1971.1.1.1.
The Experimental Studies on Cardiac Glycoside(Ouabain) and Electrolytes
- KMID: 1659309
- DOI: http://doi.org/10.4070/kcj.1971.1.1.1
Abstract
- Acute digitalization with ouabain were performed 28 times in 20 intact Mongrel dogs, who were devided into four groups : i.e. 1) Control group; Acute digitalizations were performed to observe the changes of the plasma potassium and sodium concentrations and the concomittent electrocardiographic findings. 2) Group 1;-Electrolyte solution, either KCl or NaCl, was infused during acute digitalization to observe the influences of these ions on the actions of cardiac glycoside, especially arrhythmia producing action. 3) Group 2 ; -The K depleted group and the Na depleted group was each made by the measure of diet control and the usage of oral diuretics to observe the influences of the state of depleted electrolyte (K or Na) on the action of cardiac glycoside during acute digitalization. 4) Group 3 ; -The intravenous infusion of either KCl or NaCl solution was introduced as the cardiac arrhythmia by the ouabain was produced to observe the effects of these ions on the digitalis induced arrhythmia. The results obtained were summarized as follows. (1) The arterial plasma concentration of potassium was increased during acute digitalization. The rise occurred at early stage, and the maximal increase of potassium was observed at the ventricular tachycardia. The average increase was 0.65 mEq/L as compared to control value (p<0.05). The arterial plasma concentration of sodium was reduced during acute digitalization. The fall occurred following the rise of plasma K level. The maximal reduction of sodium was observed after ventricular tachycardia, and the average decrease was 5.2 mEq/L as compared to control value (p<0.05). (2) Rapid increase up to toxic level of the plasma potassium concentration occurred occasionally during acute digitalization in the group with KCl infusion. This result was best explained due to the inhibitory action of cardiac glycoside on the K transport. (3) The interesting change was on T wave, which showed the peaking at late portion. This change occured in 60.6% during digitalization with ouabain, and paralleled mostly, but not consistently and even sometimes inversely, with the shift of plasma potassium concentration. It is tempting to assume that the change of T wave was resulted from an altered potassium gradient across the myocardial cells rather than a ssuming the changes of the plasma K level. (4) Just prior to intoxication, the marked prolongation of PR interval and ST depression were observed in about 70~80% of the cases studied. These changes might be applicable to a clue of the cardiac glycoside overdosage. (5) The intravenous infusion of KCl suppressed markedly the arrhythmia producing action of the cardiac glycoside, and resulted in prompt and dramatic abolishing, of digitalis induced arrhythmia. The intravenous infusion of KCl solution, however, produced A-V block or dissociation occasionally. This finding would be likely resulted from the additive or synergistic action of K and cardiac glycoside in suppressing A-V conducting system. (6) The NaCl infusion affected nothing to the arrhythmia producing action of cardiac glycoside. (7) The K depletion reduced markedly the threshold of the heart to the toxic effects of cardiac glycoside. (8) Potent diuretics in the state of deficient diet would produce clinically significant hypopotassemia and hyponatremia or both. The inducced hypopotassemia may provoke serious cardiac arrhythmia in the digitalized patients or animals.
