In dogs, rapid intravenous administration of large doses of amphotericin B promptly caused significant increases in serum potassium and decreases in serum sodium concentrations. In dogs which died, elec-trocardiographic tracings demonstrated a characteristic sequence of changes leading to ventricular fibrillation. It was concluded that amphotericin B causes damage to cellular membranes with resultant shift of intracellu-lar potassium into the plasma. Hydrocorti-sone mitigated the cardiac toxicity, but did not alter the hyperkalemic effect. Dogs which received smaller doses of drug for longer periods of time showed no changes in serum sodium, potassium or calcium concentration, As azotemia developed, however, serum magnesium concentrations increased significantly. In patients, amphotericin B was given during infusions of 2 hours' duration to patients who previously had received drug for several months. In most cases the serum concentration and renal clearance of electrolytes were similar to control infusions without drug. However, the serum magnesium concentration tended to decrease after drug infusion more so than after control infusion. There was no measurable increase in urinary magnesium clearance. One patient with hypokalemia showed excessive urinary potassium excretion which increased further during infusion of amphotericin B.
|Original language||English (US)|
|Number of pages||7|
|Journal||Proceedings of the Society for Experimental Biology and Medicine|
|State||Published - Sep 1964|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)