Recovery Of Gastric Secretion Research Articles

Vagal regeneration after parietal cell vagotomy: An experimental study in dogs

AbstractThe gradual increase with time of the insulin‐stimulated acid output, after a well‐performed parietal cell vagotomy (PCV), has been thought to be produced by regeneration of the vagus nerves. A genuine regeneration of the gastric branches of the vagus connected to the intramural plexus has yet to be confirmed. Experiments have been carried out in dogs to determine if this type of regeneration takes place after PCV.The animals were divided into 3 groups (A, B, and C) of 4 mongrel dogs each. In all dogs, a PCV was performed and the Grassi test was used intraoperatively to check the completeness of vagotomy. During the experiments, an insulin stimulation test and a macroscopic and microscopic study of the esophagus and stomach were obtained at several points in time (in group A, at operation and after 2 weeks; in group B, after 6 months; and in group C., after 2 1/2 years).We found, 2 weeks after PCV, a complete degeneration pattern of the vagal branches in the gastric serosa. After 6 months, and more completely after 2 1/2 years, many nerve fibers are seen, macroscopically, crossing from the vagus nerves and the branches of Latarjet to the esophagus and the lesser curvature through the old ligatures. This regeneration can be confirmed microscopically. These pathological changes in the nervous system of the stomach were found to correlate with recovery of gastric secretion. It is suggested that the recovery of acid secretion after a well‐performed PCV is accounted for by vagus nerves regeneration.

Recovery of gastric acid after vagotomy with and without a drainage.

This study tests the possibility that the difference in acid reduction after parietal cell vagotomy (PCV) and selective gastric vagotomy with a drainage (SGV + D) could be explained by differences in the secretion recovered rather than by real secretory differences. A method for estimating the completeness of aspiration during gastric function tests using the isotope Na251CrO4 as an inert marker is described. The method was used in patients with the two types of vagotomy and the recovery of gastric secretion was more complete after PCV (89.7%) than after SGV + D (75.1%). This difference may substantially account for the apparent difference in reduction of acid secretion after the two operations. The pyloroplasty supplementing the SGV is probably responsible for a pyloric loss causing a lower recovery after this operation.

The influence of secretin on the secretion of pepsin in response to acid stimulants in the anaesthetized cat.

Peptic secretion was studied in fasting anaesthetized cats in which the pylorus and common bile duct had been occluded to prevent the release of duodenal hormones which might stimulate or inhibit gastric secretion. Dilute acid was instilled into the stomach at intervals to aid recovery of gastric secretion and to preserve peptic activity. 2. Caerulein, histamine and N-methyl histamine did not increase the output of pepsin when given on their own. Desulphated caerulein was a weak peptic stimulant. 3. Two C.H.R. u./kg per hour secretin initiated pancreatic secretion, the volume of which increased progressively as the dose was increased by stages to 32 C.H.R. u./kg per hour. 4. Four C.H.R. u./kg per hour secretin did not increase the output of pepsin. Peptic secretion was stimulated by 8 C.H.R. u./kg per hour. A maximal output of approximately 2000 u. pepsin/15 min was obtained when 16 C.H.R. u./kg per hour was infused. 5. When each acid stimulant was infused along with 4 C.H.R. u./kg per hour secretin the output of pepsin increased significantly. The peak output, which usually occurred between 15 and 30 min after stimulation, did not exceed 1000 u. pepsin/15 min. 6. The proposed explanation for the potentiation of the peptic response when an acid stimulant is infused along with a dose of secretin, in itself below the threshold of peptic stimulation, is that each acid stimulant increases gastric mucosal blood flow, approximately doubling the effective concentration of secretin delivered to the peptic cell.