Code, Charles F.

Thoracic-duct lymph was collected from dogs during various phases of gastric secretion. The lymph samples were injected intravenously into dogs with vagally innervated and denervated pouches while these were secreting at slow rates in response to the continuous intravenous injection of small quantities of histamine. About half the samples inhibited gastric secretion. The rest produced transient stimulation or had no effect. The greatest degree of inhibition occurred when lymph collected immediately after a meal was injected. When fatty lymph was separated into fat and nonfat fractions, the fat-containing portion of lymph stimulated gastric secretion slightly, while the nonfat fraction carried the inhibitory influence when it was present. Systemic reactions were noted in one-third of the animals that had an inhibitory response. The occurrence of stimulatory or inhibitory factors in the lymph did not appear to be related to particular phases of gastric secretion.

Rates of insorption of radiosodium and radiopotassium from the unobstructed small bowel of rats were determined and compared with those obtained by others in healthy humans. Insorption of the isotopes under study was estimated by integration of their rates of appearance in the blood after placement in the small bowel and their rates of disappearance from blood after injection into the circulation. The rates of disappearance from arterial blood were determined during separate tests. They followed an exponential pattern similar though not identical with that reported from other species by other investigators. Radiosodium was insorbed more rapidly than radiopotassium. Mean values indicated that 50% of administered radiosodium was insorbed within 6–7 min, whereas 26–27 min were required for insorption of 50% of the radiopotassium. The rate constant during insorption of the first 76% of the Na22 was 10.8% per min and that for insorption of 58% of the K42 was 2.7% per min.

A study was undertaken to determine the effect of thiamine deficiency on the hydrochloric acid output of vagally denervated gastric pouches (Heidenhain-type) and vagally innervated gastric pouches (Pavlov-type) in dogs. Responses of both types of pouches to injection of 0.05 mg of histamine/kg of body weight and the maximal secretory capacity of both types after histamine were unaltered during the deficiency state. A degree of thiamine deficiency sufficient to produce anorexia and neuritis was without effect on the secretory response of canine gastric mucosa to histamine. The hydrochloric acid output of vagally innervated pouches during nervous stimulation caused by insulin-induced hypoglycemia was drastically reduced as soon as thiamine deficiency developed, while the response to bethanechol chloride was little, if at all, affected. It is concluded that the vagal secretory mechanism participates in the general neural failure of thiamine deficiency and that this failure most likely is in the neurons of the vagal nuclei.

Simultaneous determinations of the hourly outputs of free histamine in the urine and free acid in the juice from Heidenhain gastric pouches were made in dogs after the ingestion of meat. The gastric secretory response to the meal was separated into intestinal and gastric components. The rough parallelism, noted by others, between the outputs of acid in the gastric juice and free histamine in the urine after the meal was verified. When the meat was placed in the jejunum the output of histamine in the urine promptly increased while the output of acid was minimal or absent. Later, the output of acid increased while the output of histamine declined. Meat placed in the isolated stomach produced active secretion of acid but no increase in urinary histamine. No increase of urinary histamine followed a meal of bread and milk. During nervous secretion induced by insulin hypoglycemia, the output of free histamine in the urine did not change.

A study was undertaken to determine whether the concentration of histamine in the gastric mucosa changes with feeding, with histamine or vagal stimulation, or after the administration of cortisone. The concentration of histamine in the gastric mucosa was determined in dogs in the fasting state, after ingestion of a meal, after a meal followed by the injection of histamine, during insulin-induced hypoglycemia, and after administration of cortisone. Comparison of the different groups with the fasting series disclosed that no significant change in the mucosal concentration of histamine occurred after the meal, after the meal plus injections of histamine, or after administration of cortisone. Insulin-induced hypoglycemia caused a rise in the concentration of histamine in the mucosa of the body and antrum of the stomach.

This study was done to determine whether, after a meat meal, the outputs of acid in gastric juice and free histamine in urine are related and whether the output of free urinary histamine is increased after transplantation of the gastric antrum to the colon. Dogs with separated gastric pouches (Heidenhain) were used. Gastric juice and urine were collected at hourly intervals before and after the ingestion of the meal and for 24-hour periods before and after transplantation of the gastric antrum to the colon. Similar collections were made when histamine was injected intravenously at different rates. A rough temporal correlation was found between the outputs of HCl in gastric juice and free histamine in the urine after the meal of meat. There was not a significant increase in the 24-hour output of free histamine in the urine of the dogs in which a modest hypersecretion developed following transplantation of the gastric antrum to the colon.