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Journal of Pharmacology And Experimental Therapeutics, Vol. 158, Issue 1, 115-127, 1967
Copyright © 1967 by American Society for Pharmacology and Experimental Therapeutics

THE PATHOPHYSIOLOGY OF ACUTE AMPHETAMINE POISONING WITH PATHOLOGIC CORRELATION

Edwin G. Zalis 1, George D. Lundberg 1, and Richard A. Knutson 1

1 Research and Development Service, Department of Medicine and Pathology Service, Letterman General Hospital, San Francisco, California

Physiologic studies were performed in unanesthetized dogs administered a lethal intravenous dose of amphetamine. Various parameters were serially measured including temperature, respiratory rate, tidal volume, minute volume, oxygen utilization, left ventricular pressure, right atrial pressure, aortic pressure, cardiac output, stroke volume, peripheral resistance, arterial pH, PO2, pCO2, serum electrolytes, lactic and pyruvic acid, serum transaminase, blood glucose, blood urea nitrogen and complete blood count. A number of pathophysiologic mechanisms were observed, including a hypermetabolic state, hyperpyrexia, lactic acidemia, acidosis, shock, tachycardia, intravascular hemolysis, anoxia and ventricular outflow obstruction. Postmortem studies demonstrated a generalized hemorrhagic phenomenon with a striking involvement of the subendocardium. Also present were neuronal ganglion cell degeneration and myocardial necrosis, as well as renal vascular, pulmonary and hepatic congestion. The pathologic and physiologic changes that occurred in these animals were similar to those described in animals dying from experimental hyperthermia. It is proposed that the lethal effect of amphetamine relates to the marked hypermetabolic state which is produced by toxic doses.

Submitted on December 15, 1966
Accepted on May 2, 1967




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Copyright © 1967 by the American Society for Pharmacology and Experimental Therapeutics.