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Biomedical subjects

P L Rayford

Publications and source records attributed to P L Rayford.

At least 127 records · Page 7Linked to original sources
PubMed1978

The effect of fat on secretin release.

The effect of graded doses of intravenously infused secretin and intestinally perfused sodium oleate and HCl on pancreatic exocrine secretion and plasma secretin was determined in cats and dogs prepared with pancreatic fistulas. The pancreatic dose--response curves for bicarbonate following duodenal perfusion of oleate and HCl in cats were almost identical and paralleled the response to exogenous secretin. Although the bicarbonate response to oleate in dogs was less pronounced than the response to HCl or secretin, the bicarbonate output was observed to increase relative to protein output with increasing doses of the intestinally perfused fat. These observations suggested that secretin or a substance with secretin-like activity may be released from the intestine on contact with fat. The inability to detect changes in secretin immunoreactivity in both cats and dogs with increasing doses of oleate suggests that if secretin is released, it is in amounts undetectable by our radioimmunoassay or that some other unknown substance with secretin-like activity may be released.

Animals↗
PubMed1978

Effect of selective proximal vagotomy and truncal vagotomy on gastric acid and serum gastrin responses to a meal in duodenal ulcer patients.

To assess the effectiveness of selective proximal vagotomy (SPV) in reducing the acid response to food, we have compared pre- and postoperative gastric acid and serum gastrin responses to a meal in 11 duodenal ulcer patients with intractable pain treated by SPV, with those of seven ulcer patients with gastric outlet obstruction treated by truncal vagotomy and drainage (TV + D). Acid secretion was measured by an intragastric titration method which measures acid response to food within the stomach (5% amino acid meal) adjusted to various pH levels (5.5, 2.5, and 1.5). Studies were performed before and two to six weeks after operation. The preoperative intragastric acid output (IGAO) was about 50% of maximal acid response to Histalog. The mean preoperative IGAO at pH 5.5 For 11 SPV patients was 17.4 +/- 3.1 mEq/hour; this was decreased by 72% to 4.3 +/- 1.1 mEq/hour after operation. The mean IGAO at pH 5.5 in nine patients treated by TV + D was 21.6 +/- 3.4 mEq/hour; this was decreased by 67% to 7.3 +/- 2.1 mEq/hour. Gastrin levels were significantly higher in postop than in preop SPV PATIENTS EVEN THOUGH PH values were constant. Gastrin levels were higher in postop TV + D patients than in postop SPV patients. This study demonstrates that acid reduction achieved by SPV is reliable and at least comparable with that achieved by turncal vagotomy. Postoperative elevation of gastrin in the SPV patients suggests that the vagus may release a humoral inhibitor of gastrin release from the gastric fundus; there may also be a further direct vagal inhibitor of antral gastrin release.

Adult↗
PubMed1978

Physiologic release of secretin measured in peripheral and portal venous blood of dogs.

The effect of food on circulating levels of secretin, measured by radioimmunoassay, was studied in 7 dogs. Significant postprandial increases in secretin were found in portal and peripheral plasma of dogs fasted for 18 h. Basal levels of secretin were significantly lower in dogs fasted for 72 h when compared with dogs after an 18-hour fast. After the prolonged fast, food caused a significant release of secretin, measured peripherally. We conclude that secretin is released by a physiologic stimulus (food) and that circulating levels of secretin are depressed after prolonged starvation.

Animals↗
PubMed1978

Effect of duodenal fat on plasma levels of gastrin and secretin and on gastric acid responses to gastric and intestinal meals in dogs.

The effects of duodenal instillation of sodium oleate (10 mmoles per hr) on plasma levels of gastrin and secretin and on gastric acid secretion in response to gastric and intestinal meals were determined. Four dogs prepared with a septum between stomach and duodenum were provided with a special cannula that allowed separate access to the stomach or duodenum. Each dog received a 10% liver extract meal introduced either into the stomach (gastric phase) or into the duodenum (intestinal phase). Sodium oleate administered during the gastric phase caused approximately a 30% reduction in plasma gastrin level and a 25% inhibition of gastric acid secretion. Sodium oleate given during the intestinal phase completely abolished the plasma gastrin response and resulted in a 75% inhibition of gastric acid secretion. Plasma secretin levels were not changed during the gastric phase or the intestinal phase by instillation of sodium oleate. These results show that fat in the duodenum is a potent inhibitor of gastrin release and gastric acid secretion; the intestinal mechanism involved does not appear to affect plasma secretin concentrations.

Animals↗
PubMed1978

Concentrations of gastrin and secretin in the alimentary tract of the cat.

The distribution of gastrin and secretin in the alimentary tract of the cat was determined from the esophagogastric junction to the ileocecum. The total content and concentration of each of these hormones in mucosal extracts taken from the gastric fundus, gastric antrum, proximal and distal duodenum, proximal and distal jejunum, and ileum were measured with specific radioimmunoassays. The gastric antrum contained the highest concentration of gastrin, but appreciable amounts also were found in the duodenum. The highest concentrations of secretin were found in the duodenum, but impressive quantities were measured in the jejunum. The role of extra-antral gastrin and of those stores of secretin beyond the proximal duodenum (where the pH probably never falls to levels associated with release of secretin) currently are unknown.

Animals↗
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↗
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

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↗