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1. Salicyl compounds are readily absorbed from the stomach. 2. Gastric absorption is more rapid with the smaller salicyl molecules and at lower pH’s. 3. Calcium gluconate which does not materially affect the pH of the acetylsalicylic acid solution likewise does not affect the rate of gastric absorption. 4. Sodium bicarbonate and magnesium oxide which raise the pH of the solution inhibit the rate of gastric absorption of acetylsalicylic acid. 5. The rate of intestinal absorption of salicyl compounds is less affected by the pH of the solution than is their rate of gastric absorption. 6. Substances used to protect against gastro-intestinal irritation, such as calcium gluconate, sodium bicarbonate, and magnesium oxide, do not markedly influence the rate of intestinal absorption of acetylsalicylic acid. 7. Sodium salicylate, calcium salicylate and salicylic acid are absorbed from the intestine at a faster rate than is acetylsalicylic acid.

1. The incidence of gastric anacidity after histamine in a series of 45 healthy Rhesus monkeys was 17.7% and was higher in the female (22.2%) than in the male (13.0%).

1. Experimental acute intestinal distention in nembutalized dogs caused a reflex inhibition of the bile flow. Intraenteric pressures of 20 and 40 mm. of mercury resulted in a decrease in the bile flow of 7 to 42 per cent below the control level. 2. A decrease in the portal blood flow and oxygen supply to the liver produced by distention of the entire intestine to pressures of 70 mm. of mercury caused a further decrease in bile flow in 4 of our dogs. Oxygen therapy lessened this inhibition in all of the dogs treated. 3. Nervous reflex inhibition of the flow of urine did not occur upon distention of the small intestine to pressures of 20, 40, 60 and 90 mm. of mercury. An increase in urine flow from 11 to 81 per cent occurred. This was attributed to an increased blood flow through the kidneys. 4. The blood pressure was not significantly altered by distention of the small intestine. 5. The depth of respiration was decreased and the rate was increased by distention. Oxygen therapy decreased the respiratory rate and lessened the depression of bile flow produced by distention of the small intestine. 6. Inhibitory nervous reflexes, decreased blood flow and anoxemia probably are factors involved in decreasing liver function and thereby make the liver more susceptible to damage in cases of intestinal distention. 7. Inhibition of liver function probably precedes inhibition of kidney function in the hepatorenal syndrome of intestinal obstruction.

1. In some normal human subjects and normal dogs, single oral doses (1–2 gms.) of acetylsalicylic acid caused gastric retention; the addition of calcium gluconate tended to increase the degree of retention while the addition of sodium bicarbonate increased the rate of gastric evacuation.

1. Prolonged daily administration of acetylsalicylic acid (0.15 Gm. per kilo twice a day) resulted in digestive disturbances, alterations of nitrogen metabolism and a tendency toward acidosis in dogs. The average total nitrogen output on continued medication was decreased 11% below normal during the first twenty days, 6.2% below normal during the following twenty-five days and was increased to 15.2% above normal during the following fourteen days. “Acidosis” was evidenced during the first two periods by a decreased plasma-carbon-dioxide-combining power, an acid urine and a decreased ammonia coefficient.

1. Inhalation of 15 per cent oxygen in nitrogen for 30 to 45 minutes resulted in a 16 to 50 per cent decrease in the flow of bile below normal and a 13 to 69 per cent decrease in the flow of urine below normal in 10 nembutalized dogs. 2. Inhalation of mixtures of 10 and 5 per cent oxygen with nitrogen caused a further decrease in the flow of bile and urine. Acholia developed in 2 dogs and anuria in 5 dogs. 3. The inhalation of 100 per cent oxygen for 30 to 45 minutes after the anoxemia resulted in an increase in the flow of bile and urine above that observed during the anoxemia. In 3 dogs the flow was increased above the normal control level. 4. Mild anoxemia may be a predisposing factor in the hepatorenal syndrome of intestinal obstruction, hyperthyroidism and burns. The moderate inhibition of liver and kidney function may make these organs more susceptible to other injurious agents. 5. Severe anoxemia may be a direct causative factor because it produces a severe impairment of liver and kidney function and in some instances it may produce an acholia and anuria.

Summary and Conclusions1. Six out of 12 Rhesus monkeys failed to secrete free acid in their gastric juice 45 to 60 minutes after subcutaneous injections of 0.5 mg. histamine while 5 out of 12 failed to respond to 1.0 cc. of a preparation of “gastrin”. 2. Three out of 12 monkeys were refractory to 1.0 mg. of histamine and to 2.0 cc. of the “gastrin”preparation. 3. The “gastrin extracts”of hog's pyloric mucosa did not contain a substance capable of stimu-lating acid gastric secretion other than histamine, both in the normal and anacid monkeys. 4. None of the 12 monkeys secreted free acid in the gastric juice in response to 7% alcohol or to a meal of farina gruel and boiled potatoes.

Conclusions(1) Methylhistamine and histamine are equally potent in stimulating the gastric glands to secrete acid. (2) Methylhistamine and histamine cause a similar fall in the blood pressure in the dog. (3) Hydroxyethylglyoxaline has no effect upon gastric secretion and blood pressure in the dog.

"Anoxemia not only stops the machine but wrecks the machinery." Only a great pioneer in the study of respiration like Haldane 1 could have spoken such truth. His words should be foremost in the mind of every surgeon dealing with a patient in shock. They should be foremost in the mind of every anesthetist dealing with a narcotized patient, because asphyxia is one of the dangers present in all forms of anesthesia. The health and the very life of the patient depend on the surgeon's knowledge and skill in preventing and averting anoxia. The number of deaths under anesthesia is appalling. Jarman 2 collected statistics from the hospitals of all the English-speaking countries. He received detailed reports of nearly 1,300 deaths under anesthesia between 1921 and 1939. Of this series of approximately 1,300 detailed cases the following classifications were made: When the anesthetic was specified the number of deaths under

Since Tainter and Stockton's 1 original report on the effectiveness of neo-synephrin as a systemic vasoconstrictor stimulant, its use as a vasopressor drug for spinal anesthesia has been reported by numerous investigators. 2 These workers have reported its effect in elevating and sustaining the blood pressure during spinal anesthesia. The associated bradycardia has also been discussed thoroughly. The action of neo-synephrin on the respiration has been briefly commented on by Tainter and Throndson 3 and by Tainter, Throndson and Moose 4 in conjunction with its use in solutions of procaine hydrochloride as a local anesthetic for dental nerve blocking. Their results indicated that the action of neo-synephrin on the respiration is not of great clinical significance. Data relative to the effects of neo-synephrin on urinary excretion are meager. Boyd 5 reported that 0.5 cc. of a 0.01 per cent solution of neosynephrin hydrochloride caused a marked antidiuretic action analogous to