TY - JOUR
T1 - Electrocardiographic and Electrolyte Abnormalities Caused by Amphotericin B in Dog and Man
AU - Butler, William T.
AU - Bennett, John E.
AU - Hill, George J.
AU - Szwed, Clarence F.
AU - Cotlove, Ernest
PY - 1964/9
Y1 - 1964/9
N2 - 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.
AB - 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.
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U2 - 10.3181/00379727-116-29391
DO - 10.3181/00379727-116-29391
M3 - Article
C2 - 14230372
AN - SCOPUS:0010348619
VL - 116
SP - 857
EP - 863
JO - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)
JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)
SN - 0037-9727
IS - 4
ER -