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 digitalization were performed to observe the changes of the plasr4a .potassium and sodium concentrations and the concomittent electrocardiographic findings.
2) Group 1;-Electrolyte solution, either KCI 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 KCI 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 couLpared 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 KCI 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 shifts of plasma potassium concentration.
It is tempting to assume that the change of T wave was resulted from an altered potassiunm gradient across the myocardial cells rather than assuming to changes of the plasma K Ievel.
④ Just prior to intoxication, the marked prolongation of P-R interval and S-T depression were observed in about 70805vo of the cases studied. These changes might be applicable to a clue of the cardiac glycoside overdosage.
⑤ The intravenous infusion of KCi 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 KCI solution, however, produced A-V block or dissociation occasionally.
This finding would be likely resulted from the additive or synergistic actions of K and cardiac glycoside in suppresshig 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 diuretic2 in the state of deficient diet would produce clinically significant hypopotassemia and hyponatremia or both.
The inducced h.y popotassemia may provoke serious cardiac arrhythmia in the digitalized patients or animals.
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