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A study of the experiments comprising the first group of animals permits the deduction that these animals succumb to the acute poisoning as a result of the shock which the poison induces through its corrosive action in the stomach and intestine. The animals die before the mercury, acting as such during its elimination by the kidney, can induce an acute nephropathy and before the mercury, by inducing an acid intoxication, can lead to an acute kidney injury. The remaining animals of the series, Groups II, III, and IV, have withstood the corrosive action of the poison. These animals have shown the same type of delayed intoxication from the poison. The intoxication, however, has varied in time of appearance, duration, and severity. The animals classified as Group II have developed during the stage of improvement from the gastroenteritis a rapid and severe type of acid intoxication, have become rapidly anuric, and have died either in a state of air-hunger or in convulsions. The animals of Group III, either during or after their recovery from the gastroenteritis, have developed a mild grade of acid intoxication. During the following days of the experiments the animals succeeded in reestablishing their normal acid-base equilibrium. All the animals of this group recovered. The animals of Group IV have shown a recovery from the mercury enteritis. Following a period during which there was an attempt on the part of the animals to return to normal, as indicated by an increase in the alkali reserve of the blood and by an increased output of phenolsulfonephthalein and urine, the members of the group developed a delayed acid intoxication, and, like the animals of Group II, became anuric.

A STUDY OF ACUTE MERCURIC CHLORIDE INTOXICATIONS IN THE DOG WITH SPECIAL REFERENCE TO THE KIDNEY INJURY