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Biomedical subjects

P L Rayford

Publications and source records attributed to P L Rayford.

At least 91 records · Page 5Linked to original sources
PubMed1983

Release of cholecystokinin in conscious dogs: correlation with simultaneous measurements of gallbladder pressure and pancreatic protein secretion.

We have used an antibody that cross-reacts with cholecystokinin-33/39 to measure cholecystokinin release into plasma; this release was correlated with simultaneous measurements of gallbladder pressure and pancreatic protein secretion in response to intestinal administration of fat. Nine conscious dogs were prepared with chronic gastric, pancreatic, and gallbladder fistulas. Plasma cholecystokinin, gallbladder pressure, and pancreatic protein output were measured simultaneously before, and at intervals during, a 2-h intraduodenal infusion of sodium oleate. This infusion resulted in significant (p less than 0.05) elevations of plasma cholecystokinin (from 64 +/- 7 to 181 +/- 27 pg/ml), in gallbladder pressure (from 13 +/- 1 to 27 +/- 3 cmH2O), and in pancreatic protein output (from 65 +/- 7 to 148 +/- 21 mg/15 min); all measurements are from the basal state to 120 min after the onset of duodenal perfusion. Plasma concentrations of cholecystokinin were significantly correlated with gallbladder pressure (r = 0.91, p less than 0.05) and pancreatic protein output (r = 0.84, p less than 0.05). These data provide evidence that release of endogenous cholecystokinin, as measured by radioimmunoassay, can be correlated with the classic biologic actions ascribed to cholecystokinin.

Animals↗
PubMed1982

Removal of circulating gastrin and cholecystokinin into the lumen of the small intestine.

This study was undertaken to investigate the mechanism by which the small intestine removes circulating gastrin and cholecystokinin (CCK). A 100-cm (acute study, 10 dogs) or a 50-cm (chronic study, 5 dogs) segment of midjejunum was excluded in all 15 dogs. The excluded loop was perfused with 0.1 M phosphate buffer (pH 7.4), which was constantly recirculated by a peristaltic pump. It the acute control study (5 dogs), gastrin concentrations in the intestinal perfusate were increased gradually to a level of 320 +/- 49 pg/ml at 90 min (i.e., 7.6 +/- 0.9 times higher than serum gastrin levels). In the antrectomy group (5 dogs), perfusate gastrin concentrations were greatly decreased after antrectomy, in consonance with the decrease in serum gastrin concentrations. In the chronic study (5 dogs), perfusate gastrin concentrations were significantly increased after food stimulation, in consonance with the increase in serum gastrin concentrations. CCK was also released into the bowel lumen in considerable amounts basally and after endogenous release. Although one cannot exclude the possibility that a considerable amount of gastrin or CCK in the lumen may originate from the bowel segment, this study shows that the small bowel removes gastrin and CCK from the circulation by their secretion into the bowel lumen. Loss of this mechanism might partially explain the rise in gastrin levels that is observed in some patients after extensive small bowel resections.

Animals↗
PubMed1982

Effect of cigarette smoke on human serum trypsin inhibitory capacity and antitrypsin concentration.

Investigation of the effect of cigarette smoke on the serum trypsin inhibitory capacity (TIC) and antitrypsin content in 89 smokers compared with 37 nonsmokers revealed that cigarette smoking is associated with a significantly lower level of TIC. No alteration in serum antitrypsin content was found because of cigarette smoking. Further analysis of the data indicated a correlation between the magnitude of smoking and the reduction in serum TIC. The reduction of TIC in cigarette smokers is consistent with the recent findings of decreased alpha 1-antitrypsin activity in rat lung and the reduced elastase inhibitory capacity per mg of alpha 1-antitrypsin found in the serum of smokers. The decrease in TIC in the serum of smokers, in addition to the reported decrease in elastolytic activity, may be useful in explaining the pathogenesis of emphysema frequently found in smokers.

Adult↗
PubMed1982

Reduction of postprandial release of pancreatic polypeptide after development of pancreatic fibrosis.

We have measured the plasma pancreatic polypeptide response to a meal before and after the development of pancreatic fibrosis in dogs. Peripheral blood samples were collected in five dogs before and after a standard meal for measurement of pancreatic polypeptide by a specific radioimmunoassay. The next day, all of the pancreatic ducts were ligated in each dog, and one month after pancreatic ductal ligation, the food study was repeated. The dogs were sacrificed on the following day, and the pancreas of each dog was studied morphologically. Before pancreatic ductal ligation, plasma pancreatic polypeptide concentrations showed a biphasic response to a meal; a primary, rapid increase lasted 30 to 45 minutes, and a secondary, prolonged increase lasted for more than 180 minutes. One month after pancreatic ductal ligation, plasma concentrations of pancreatic polypeptide, at each time period during the initial 60 minutes after food, were significantly less than the corresponding sample before pancreatic ductal ligation. The total amount of pancreatic polypeptide released after a meal during the initial 60 minutes was diminished significantly by pancreatic ductal ligation. Neither plasma concentrations of pancreatic polypeptide nor the total amount of pancreatic polypeptide release after a meal showed a significant change during the last 180 minutes after food. Results of histologic observations showed destruction and fibrotic replacement of the acini of the pancreas after ligation of the pancreatic ducts. The islets were well preserved. Since the cells of origin of pancreatic polypeptide are distributed in both the acini and islets of the pancreas in dogs, we suggest that the primary, rapid phase of pancreatic polypeptide after a meal may be derived chiefly from cells in the acini, whereas the secondary phase of response may be derived chiefly from cells in the islets.

Animals↗
PubMed1982

Release of antral gastrin in response to an intestinal meal in dogs.

This study was designed to determine whether gastrin is released by the antrum in response to an intestinal meal in dogs. Two groups of anesthetized dogs were prepared with innervated antral pouches. The antrum and duodenum were separated by complete division at the pylorus to prevent duodenoantral reflux. The duodenum and proximal jejunum were perfused with 10% liver extract at 200 ml/hr. In one group of six dogs a significant elevation of antral vein gastrin levels was observed after 45 minutes. Gastrin levels in portal and peripheral blood were not significantly elevated. In another group of eight dogs, in which antral veins were not cannulated, a significant rise in peripheral gastrin concentration was noted after 60 minutes. We conclude that gastrin is released by the antrum during the intestinal phase of gastric acid secretion; significantly increased levels of gastrin are detected in both antral and peripheral venous blood. Duodenoantral reflux, as a possible cause of this release, is ruled out by complete surgical separation between duodenum and antrum.

Animals↗
PubMed1981

Pancreatic polypeptide. A review.

Pancreatic polypeptide (PP), 36-amino acid peptide, may function as an important feedback inhibitor of pancreatic secretion after a meal. It arises from both islet and acinar cells of the pancreas. Release of PP by a meal, primarily protein, occurs in a biphasic manner. The first rapid release occurs as a result of vagal stimulation; the second, more prolonged rise (the so-called intestinal phase) occurs in response to hormonal stimulation, predominantly cholecystokinin. Plasma PP levels increase with age; PP levels are elevated above those of age-controlled normal subjects in diabetic patients and in some patients with pancreatic amine precursor uptake decarboxylase tumors. The value of plasma PP as a possible marker for pancreatic tumors is as yet unsettled but may be a valuable tool.

Animals↗
PubMed1981

Does luminal gastrin stimulate gastric acid secretion?

The effects of pentagastrin on acid secretion, short circuit current, electrical conductance and potential difference were determined in isolated bullfrog fundic mucosa. Biologically active luminal pentagastrin had no effect on gastric mucosa, even at a concentration 100 times higher than that necessary for stimulation of the mucosa from the serosal side. It is concluded that luminal gastrin does not appear to have a physiologic role in gastric secretory processes.

Animals↗
PubMed1981

Radioimmunoassay study of hepatic clearance and disappearance half-time of somatostatin and vasoactive intestinal peptide in dogs.

The effects of hepatic transit on concentrations of synthetic cyclic (ovine) somatostatin and of highly purified (porcine) vasoactive intestinal peptide were studied in five conscious dogs prepared with indwelling portal catheters. The peptides were infused via peripheral vein catheters or the portal catheters for 40 minutes at actual integrated doses of 2.8 pmol/kg/min for vasoactive intestinal peptide an 8.2 pmol/kg/min for somatostatin. Specific radioimmunoassays were used for the measurement of the circulating peptides. As estimated from the plateau peptide concentrations achieved a hindleg vein during the portal and the peripheral infusions, the transhepatic loss of immunoreactive vasoactive intestinal peptide was 72.9 +/- 2.1%, against 27.5 +/- 12.5% for somatostatin. For the given doses of peptides infused systematically, the half-life, metabolic clearance rate, and distribution volume were, respectively, 1.80 +/- 0.1 minutes, 39.3 +/- 5.2 ml/kg/min, and 103.7 +/- 14.8 ml/kg for vasoactive intestinal peptide, and 1.0 +/- 0.2 minutes, 95.2 +/- 12.5 ml/kg/min, and 114.7 +/- 6.0 ml/kg for somatostatin. These results indicate that (ovine) somatostatin and (porcine) vasoactive intestinal peptide are both readily cleared from plasma in dogs. In the present experimental conditions, vasoactive intestinal peptide, but not somatostatin, was rapidly altered through hepatic transit so that it escaped recognition by the assay system.

Animals↗
PubMed1981

Hormone-stimulated release of pancreatic polypeptide before and after vagotomy in dogs.

Concentrations of pancreatic polypeptide (PP) in peripheral blood were measured before, during, and after infusions of graded doses of synthetic human gastrin I (SHG-I), cholecystokinin 99% pure (CCK-99%), CCK octapeptide (CCK-OP), and pure natural porcine secretin in six dogs with gastric and duodenal fistulas. Studies were repeated after truncal vagotomy. Significant increases in concentrations of PP were found with 1 microgram . kg-1 . h-1 of SHG-I, 0.25 and 1.0 microgram . kg-1 . h-1 of CCK-99%, and 0.06 and 0.25 micrograms . kg-1 . h-1 of CCK-OP. Significant increases persisted after vagotomy, except at the lower dose of CCK-OP. Postvagotomy responses were significantly less than prevagotomy, except at the higher doses of CCK-99% and CCK-OP. Pure secretin did not change concentrations of PP in blood before or after vagotomy. The most potent stimulant for PP release on a molar basis was CCI-99%, followed by CCK-OP and SHG-I. The results suggest that cholinergic and humoral agents of the gastrin-cholecystokinin family interact in the normal physiological response of PP to food and that, in dogs, CCK-like peptides are more potent than gastrin.

Animals↗
PubMed1981

Action of pancreatic polypeptide on exocrine pancreas and on release of cholecystokinin and secretin.

We have studied the effect of exogenous porcine pancreatic polypeptide (PP; 0.8 and 2.1 microgram/kg . h, iv) on endogenously stimulated pancreatic exocrine secretion in five pancreatic-fistula dogs. Plasma levels of cholecystokinin (CCK), secretin, and PP were measured in addition to pancreatic secretion of water, bicarbonate, and protein. Intraduodenal infusions of acid and a mixture of phenylalanine and tryptophan were used to stimulate hormone release. PP caused a dose-dependent inhibition of endogenously stimulated pancreatic secretion, whereas the release of CCK and secretin was not affected. Duodenal acidification and intraduodenal infusion of phenylalanine and tryptophan caused a significant release of PP. This study shows that: 1) PP suppresses pancreatic secretion by means of a mechanism that is probably direct; this effect is not mediated through inhibition of release of CCK or secretin, and 2) phenylalanine and tryptophan, both strong stimulants of CCK release, cause a substantial rise in PP in peripheral blood. The mechanism of PP release may involve CCK (in previous studies, we have shown a rise in circulating PP levels after iv CCK infusion).

Animals↗
PubMed1980

Role of gastrin in vagally-stimulated pancreatic secretion.

In an attempt to clarify the contribution of antral gastrin to the vaginal stimulation of pancreatic secretion, we have measured the effect of total excision of the antral mucosa on pancreatic secretion induced by electrical vagal stimulation in eight anesthetized dogs. Stimulation was done before excision of the mucosa, and after excision, with and without a gastrin background. Mucosal excision reduced pancreatic volume response to 25% and pancreatic protein response to 32% of the respective responses obtained before excision; gastrin release in response to vagal stimulation was completely abolished. With a gastrin background (0.5 microgram/kg-hr of synthetic human gastrin-17-I), which resulted in serum gastrin concentrations higher than those obtained by vagal stimulation before excision of antral mucosa, the pancreatic volume and protein response showed only partial restoration. These studies provide evidence that vagal pancreatic secretion is only partially gastrin-dependent, and that other antral factors, probably vagally modulated intramural cholinergic pathways, are involved.

Animals↗
PubMed1980

Release of vasoactive intestinal peptide by distention of the proximal stomach in dogs.

The effect of transient proximal gastric distention was studied in six conscious dogs previously submitted to antrectomy and Billroth I anastomosis (and in which the intragastric pH was not altered), and in five anaesthetised dogs prepared with an innervated acute fundic pouch in which the pouch lumen was acidified with 0.15 M hydrochloric acid. Levels of vasoactive intestinal peptide (VIP) in portal and peripheral plasma were measured by radioimmunoassay. In conscious antrectomised dogs, distention of the proximal stomach to volumes of 250 and 500 ml evoked a significant rise of portal VIP concentration, with a maximal variation of 32.7 +/- 4.4 to 67.7 +/- 14.8 pg ml-1, which was hardly reflected in systemic blood. In the anaesthetised dogs, transient distention of the acute fundic pouch with 0.15 M hydrochloric acid under a pressure of 40 cm of water elicited a significant rise of portal VIP from 36.2 +/- 8.9 to 59.8 +/- 12.4 pg ml-1 (P < 0.05) without any significant variation of the peptide concentration in peripheral plasma. These results indicate that vasoactive intestinal peptide is released under transient proximal gastric distention in dogs, and that this response is not solely dependent upon the acid secretory effect of distention in this species.

Animals↗