Ammonium acetate (13 m-mol), ammonium bicarbonate (13 m-mol), and ammonium hydroxide (30 m-mol) were administered intravenously to three separate groups of five dogs. Ammonium acetate and bicarbonate were given over a period of 15 minutes, ammonium hydroxide was given for 30 minutes. In all dogs, after 15 minutes' infusion, the blood ammonia concentration was similar to that found in patients with hepatic coma. When the ammonium hydroxide had been given for 30 minutes, lightening of anaesthesia was noted in all dogs studied. At this time blood ammonia values were over 1,000 μg/100 ml in two animals. Subsequent deepening of anaesthesia was observed after termination of the infusion. In all animals studied there was an increase in cerebral glucose consumption with little change in oxygen utilization. Arterial lactic acid was studied in the group given ammonium bicarbonate and found to increase at the same time as the increase in glucose utilization. Hyperventilation was precipitated by both acid and alkalilne ammonium salts. Lactic acidosis appeared to be the cause rather than the result of the hyperventilation. The protective effect of hyperventilation on brain metabolism is discussed.
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