PT  - JOURNAL ARTICLE
AU  - ROZA, OTTO
AU  - BERMAN, LEONARD B.
TI  - THE PATHOPHYSIOLOGY OF BARIUM: HYPOKALEMIC AND CARDIOVASCULAR EFFECTS
DP  - 1971 May 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 433--439
VI  - 177
IP  - 2
4099  - http://jpet.aspetjournals.org/content/177/2/433.short
4100  - http://jpet.aspetjournals.org/content/177/2/433.full
SO  - J Pharmacol Exp Ther1971 May 01; 177
AB  - The ingestion of absorbable barium salts, e.g., carbonate or chloride, produces a combination of ectopic ventricular contractions, ventricular tachycardia, skeletal muscle paralysis, salivation, diarrhea, hypertension and finally, respiratory paralysis and ventricular fibrillation. Infusion of barium chloride into anesthetized dogs produced all of the above, plus a prompt and substantial hypokalemia. The data suggest that the hypokalemia is due to a transfer of potassium from extracellular to intracellular compartments rather than to urinary or gastrointestinal losses. Potassium administration prevented or reversed all of the clinical effects except the hypertension. Arterial hypertension was a constant feature of BaCI3 infusion and was not affected by simultaneous potassium infusion, by the injection of phentolamine or by bilateral nephrectomy. Barium and potassium were each found to be powerful antagonists of the other's cardiac toxicity. The intracellular accumulation of potassium induced by barium together with the reported ability of barium to stimulate myocardial adenosine triphosphatase suggests the possibility of a role for barium in the management of digitalis poisoning. © 1971 by The Williams & Wilkins Co.