The effect of salicylates on the electrolyte structure of the blood plasma. I. Respiratory alkalosis in monkeys and dogs after sodium and methyl salicylate; 'the influence of hypnotic drugs and of sodium bicarbonate on salicylate poisoning

The clinical picture typical of salicylate poison-ing has often been described: hyperpnea appears to be the most prominent symptom; other symp-toms are vomiting, thirst, sweating, diuresis, fever, and various signs of irritation of the central nerv-ous system, including convulsions followed by de-pression and coma. Albumen, casts, and red and white cells are often found in the urine. The physiologic mechanism underlying the hyperpnea of salicylism has been the subject of much discus-sion. As the dyspnea of salicylate poisoning was noted to resemble the Kussmaul type of breath-ing of diabetic coma, ketone bodies were suggested as a common cause for the acidosis and hyper-ventilation in both conditions (1). This hypothe-sis was not borne out in later studies, which did not reveal increased ketonemia in man or rabbits receiving large doses of salicylates (2). In more recent times the theory of a primary metabolic acidosis, accepted by many clinical observers, ap-peared to be supported by the finding of a de-creased bicarbonate content of the blood, but the origin of this presumed acidosis has remained obscure (3 to 5). Increased amounts of lactate found in the blood of rabbits following sodium salicylate administration were thought to be partly responsible for the presumed acidosis (6). The significance of this observation appears uncertain, since the increases varied widely, and the muscu-lar effort involved in hyperventilation may have accounted for them. A renal mechanism for the metabolic acidosis has been suggested (7, 8) but the rapidity of the onset of the hyperpnea and the inconstancy and mildness of the renal changes appear difficult to reconcile with such an hypothe-sis. Another group of observers has favored the 1 A preliminary report was presented before the Ameri