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Biomedical subjects

J C Thompson

Publications and source records attributed to J C Thompson.

At least 451 records · Page 25Linked to original sources
PubMed1978

Influence of vagus on mechanisms for stimulation and inhibition of gastrin release.

In studies in dogs the gastrin response to food, to bombesin (1 micrgoram/kg-hr), and to somatostatin (2.5 and 5.0 microgram/kh-hr) plus food before and after truncal vagotomy was determined. Vagotomy caused an increase in basal levels of gastrin and in the release of gastrin after bombesin and food. Vagotomy augmented somatostatin suppression of food-stimulated gastrin release in a dose-dependent manner. We suggest that vagotomy causes a loss of both stimulatory and inhibitory vagal effects on gastrin release. Loss of vagal inhibition results in increased gastrin release to bombesin and food. Loss of vagal stimulation results in intensification of somatostatin-induced inhibition of postprandial gastrin release.

Animals↗
PubMed1978

An impurity in the buffer 2-amino-2-methyl-1-propanol, which correlates with depression of measured alkaline phosphatase activity.

Recent findings indicate that the buffer 2-amino-2-methyl-1-propanol, widely used in clinical measurement of alkaline phosphatase activity, contains an impurity that inhibits the activity of the enzyme. Analysis of several lots of 2-amino-2-methyl-1-propanol has demonstrated the presence of a material, the concentration of which correlates well with alkaline phosphatase activity. Mass spectral analysis of this material indicates that it is a substituted ethylenediamine compound. Zinc chelation is discussed as a possible mode of its inhibition. Further work is in progress to separate and characterize this and other compounds in the buffer and to determine their modes and degrees of alkaline phosphatase inhibition.

Alkaline Phosphatase↗
PubMed1978

Hormonal influences on gastric secretion.

Gastric secretion in response to a meal is stimulated by a variety of neurohumoral agents. Acidified chyme flowing into the duodenum evokes a series of events that bring about the neutralization of H+ or suppression of further acid secretion. The actions of several proven and putative stimulatory and inhibitory agents are summarized in Figure 8.

Cholecystokinin↗
PubMed1977

The effect of glucagon on pancreatic secretion and plasma secretin in dogs.

The inhibitory effect of glucagon on pancreatic exocrine secretion induced by endogenously released secretin was studied in 4 dogs with chronic pancreatic fistulas and open gastric fistulas. After a constant level of pancreatic secretion was established by intraduodenal hydrochloric acid perfusion (9 mEq/hr), glucagon (30 microng/kg-hr) was administered intravenously for 1 hr. Compared to a separate control study in which dogs received intraduodenal HC1 alone, glucagon caused a significant decrease in both pancreatic volume flow and bicarbonate output. Glucagon had no effect on pancreatic protein secretion, and circulating levels of endogenously released secretin remained unchanged. It is concluded that the inhibitory effect of glucagon on pancreatic secretion is not mediated through inhibition of secretin release. The chemical homology between glucagon and secretin suggests that glucagon may mediate its inhibitory action by competing with secretin at the level of the pancreatic receptor site.

Animals↗
PubMed1977

The effect of nephrectomy on the catabolism of secretin.

Previous studies have shown the kidney to be an important site for the catabolism of secretin. We have investigated possible sites within the kidney for secretin uptake in four intact anesthetized dogs. The disappearance half-time of an intravenous infusion of secretin, measured by a sensitive and specific ratioimmunoassay in four intact anesthetized dogs was 2.84 minutes. After ureteral ligation (to arrest glomerular filtration), the half-time of a similar intravenous dose of secretin was 2.78 minutes. Finally, the renal vascular pedicles were ligated to totally exclude the kidneys from the circulation and the half-time was found to be 5.43 minutes. These findings demonstrate that the efficient renal mechanisms for secretin degradation are not dependent upon glomerular filtration but upon some other mechanism, presumably located in renal tubular cells.

Animals↗
PubMed1977

Emergency diagnosis of upper gastrointestinal bleeding by fiberoptic endoscopy.

Emergency esophagogastroduodenoscopy has been performed in 192 consecutive patients admitted with massive gastrointestinal bleeding. Accurate endoscopic diagnosis was made in 184 or 96%; 58 patients underwent emergency operations to control bleeding with an overall operative mortality of 26%. Excluding 16 patients who underwent emergency portacaval shunting, the operative mortality was 7%. In 6 patients, the bleeding was controlled by endoscopic electrocoagulation. There were no complications. Emergency endoscopy should be done routinely as the primary diagnostic approach in the diagnosis of upper gastrointestinal bleeding.

Adult↗
PubMed1977

Acid and endocrine responses to meals varying in pH in normal and duodenal ulcer subjects.

Recent studies suggest that duodenal ulcers may develop because of increased drive to secrete acid and decreased effectiveness of feedback mechanisms that inhibit acid output. This study was designed to compare gastric acid, gastrin, gastric inhibitory peptide (GIP) and secretin responses to meals (varying in pH) in 12 normal subjects and nine duodenal ulcer patients. Acid secretion was measured by an intragastric titration method which allows actual measurement of acid response to food within the stomach (ten per cent amino acid meal (AAM) adjusted to various pH levels, 7-1.5). Blood samples were collected at each pH level for radioimmunoassay of gastrin, secretin and GIP. Gastric acid and gastrin responses to AAM were found to be significantly greater in duodenal ulcer patients than in normal subjects. In duodenal ulcer patients, acid response to AAM at pH 7 or 5.5 reached 82% of Histalog maximum. Decreasing the pH of the meal resulted in a stepwise reduction in both acid secretion and gastrin in normal subjects and duodenal ulcer patients. At pH 1.5, acid inhibition was complete, but gastrin inhibition was partial. Secretin increased significantly at pH 1.5; there was no difference in secretin release between the groups. Plasma GIP was highest at pH 7 in all individuals. Use of a marker substance showed 80% recovery of AAM at pH 7-4; below pH 4, recovery rose to about 90%. We conclude that gastric acid and gastrin release are pH-dependent in normal and duodenal ulcer subjects. Inhibition of gastric secretion by acidified meals is associated with a pH-dependent suppession of gastrin and GIP levels and elevation of plasma secretin. This study confirms increased acid and gastrin responses in duodenal ulcer patients but shows no evidence of defective feedback inhibition of gastric secretion and gastrin release.

Adult↗
PubMed1977

Release of antral and duodenal gastrin in response to an intestinal meal.

In dogs prepared with isolated, innervated antral pouches, intraduodenal perfusion with liver extract at pH 7, with the atrum buffered at pH 7, resulted in a significant release of gastrin selectively from the antrum and from the duodenum. Acidification of the meal to pH 1 abolished both antral and duodenal gastrin release, whereas acidification of the antrum abolished only the antral gastrin response. After antrectomy, liver extract at pH 7 caused a diminished but significant release of duodenal gastrin. These studies provide evidence that an intestinal meal may release (in addition to a specific intestinal phase hormone) gastrin from the intestine, and from antrum, by means of a pH-sensitive mechanism which may involve a humoral agent (enterobombesin?) from the small bowel.

Animals↗
PubMed1977

Pancreatic bicarbonate, serum gastrin, and secretin responses to meals varying in pH.

The role of secretin in the postprandial bicarbonate response by the pancreas is not clear. This study reports secretin and bicarbonate secretion after exogenous and endogenous acidification of meal. In dogs with gastric and pancreatic fistulas, a liver extract meal at various pH levels was introduced into the stomach and kept at the preselected pH by intragastric titration. Gastric acid, pancreatic bicarbonate, serum gastrin, and plasma secretin were measured. The meal at pH 7 produced an increase of gastrin levels of 230% above basal and a gastric acid output from a basal of 0.8-16.9 meq/30 min. Acidification of the meal evoked a pH-dependent reduction of gastrin and gastric acid secretion, a pH-dependent elevation of pancreatic bicarbonate, and significant elevation of secretin at pH 3 (43% above basal) and at pH 2 (80% above basal). Postprandial endogenous acidification of a meal, without intragastric titration, also provoked significant release of secretin. Maximal pancreatic bicarbonate secretion in response to exogenous secretin was augmented 30% by the addition of a liver extract meal at pH7. It is concluded that in dogs with pancreatic fistulas, a meal exogenously or endogenously (postprandial) acidified is capable of the release of secretin in immunoassayable amounts. The normal pancreatic bicarbonate response to food may depend partially upon potentiation of the secretin effect by other neurohumoral stimuli.

Animals↗
PubMed1977

Gastrin.

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Animals↗