Search PubMed⌕ Search

Biomedical subjects

P L Rayford

Publications and source records attributed to P L Rayford.

At least 109 records · Page 6Linked to original sources
PubMed1980

Effects of gastrin on circulating levels of somatostatin, pancreatic polypeptide, and vasoactive intestinal peptide in dogs.

The effect of synthetic human gastrin I, infused at two doses, on the concentrations of somatostatin, pancreatic polypeptide, and vasoactive intestinal peptide in portal and systemic blood was studied in six anesthetized dogs. Intragastric pH was maintained at 5.5, and acid output was measured by intragastric titration. Significant increases in somatostatin and pancreatic polypeptide concentrations in portal blood were found with the lower dose of gastrin (0.5 microgram/kg . h) infused for 40 min. When gastrin was infused at 1.5 microgram/kg . h for 100 min, both portal and systemic blood concentrations of somatostatin and pancreatic polypeptide rose significantly. Cimetidine (300 mg, as an iv bolus), given 40 min after the beginning of the second infusion, did not affect gastrin-stimulated release of somatostatin and pancreatic polypeptide, whereas acid output was completely abolished. Vasoactive intestinal peptide concentrations did not change with the infusion of either dose of gastrin. This daily shows that gastrin releases somatostatin and pancreatic polypeptide in a dose-dependent fashion, and since this release was not acid mediated, it appears likely to be a direct action of gastrin.

Animals↗
PubMed1980

Immunoreactive somatostatin and vasoactive intestinal peptide in the digestive tract of cats.

Somatostatin and vasoactive intestinal peptide were measured by radioimmunoassay in acetic acid extracts of tissue samples from the digestive tracts of seven adult cats. The concentration of immunoreactive somatostatin in antral mucosa (2926 +/- 978 pmol/g wet weight, mean +/- SE) was far above the concentrations in the head of the pancreas (442 +/- 94), distal duodenum (377 +/- 91), and ileum (355 +/- 48). Large amounts of immunoreactive vasoactive intestinal peptide were recovered from both mucosal and muscular layers of gastrointestinal tract; the highest values were observed in the muscular layer of the cecum (579 +/- 82 pmol/g) and the mucosa of the right colon (564 +/- 244). The mucosal/muscular layer ratio of vasoactive intestinal peptide concentrations increased caudally from 0.20 in the esophagus to over 1 in the ileum and colon. Upon gel filtration on G-50 Sephadex, somatostatin in the antrum, duodenum, and pancreas were eluted as a predominant peak in the volume of the tetradecapeptide, but somatostatin from the ileum and cecum was associated with a major faster component. Vasoactive intestinal peptide in the muscular layer of gastrointestinal tract and in mucosa of antrum and duodenum consisted essentially of a single form, which coeluted with the purified porcine peptide; a slower component was detected in the mucosa of the ileum and cecum. These reults indicate molecular heterogeneity of both immunoreactive somatostatin amd vasoactive intestinal peptide in the digestive tract of cats, and suggest that the variable ratio of the different molecular forms of each peptide along the gastrointestinal tract may reflect regional specificity of biologic effects and metabolism.

Animals↗
PubMed1980

Effects of test meal, intragastric nutrients, and intraduodenal bile on plasma concentrations of immunoreactive somatostatin and vasoactive intestinal peptide in dogs.

Specific radioimmunoassay were used to measure somatostatin and vasoactive peptide in portal and peripheral plasma from conscious dogs prepared with indwelling portal catheters. In six animals with intact stomachs, a test meal induced a significant rise of portal and peripheral somatostatin, while the significant response of vasoactive intestinal peptide in portal plasma was not reflected in peripheral blood. Similar somatostatin and vasoactive intestinal peptide responses were observed in six dogs previously submitted to antrectomy and Billroth I anastomosis, when given the same test meal, while the gastrin response was 20% of the response in the intact dogs (P < 0.01). The effects of intragastric instillation of 300 ml dextrose, casein hydrolysate, and Intralipid, adjusted to 300 mosmol/kg and pH 7.0, were studied in six dogs with intact stomachs. Casein and Intralipid induced significant increases of somatostatin in portal and peripheral plasma, while VIP increased after Intralipid only, both in portal and peripheral blood. Dextrose resulted in no significant variation of either peptide in portal or in systemic plasma. Intraduodenal infusion of isotonic bile induced a significant release of somatostatin, both in portal and peripheral plasma, but no significant vasoactive intestinal peptide response. These results indicate that several factors can evoke a significant release of somatostatin in dogs, and that the variations of the peptide concentration in portal plasma are reflected in peripheral blood. Among the factors tested, only intragastric fat evoked a vasoactive intestinal peptide response that could be measured in peripheral blood.

Animals↗
PubMed1980

Radioimmunoassay of plasma cholecystokinin (CCK), duodenal release of CCK, diurnal variation of plasma CCK, and immunoreactive plasma CCK components in man.

A precise and specific radioimmunoassay method for measuring plasma cholecystokinin (CCK) is described. The present assay system using a stable tracer iodinated by means of a modified Chloramine-T method followed by purification on a Sephadex G-15 and a SP Sephadex C-25 column, as well as careful corrections for non-specific plasma effects, allows measurements of fasting plasma CCK in the low pmol/l range; the significant rise in plasma CCK following duodenal infusion of fat; and the significant diurnal variation of plasma CCK. Apparent immunoreactive meal-stimulated plasma CCK was eluted from a Sephadex G-50 superfine column in four fractions. The first and largest peak probably represents plasma CCK bound to plasma proteins and non-specific plasma effects, the second and smaller peak big CCK with molecular weight between some 5,000 and some 30,000, the shoulders following the second peak ordinary CCK33 and CCK39 variant, and the final, and by far the smallest peak, may possibly represent COOH-terminal tetra- (CCK4) or octapeptides (CCK8) of CCK.

Animals↗
PubMed1980

Hormonal (gastrin, secretin, cholecystokinin) and secretory effects of bombesin and duodenal acidification in dogs.

We have studied the influences of duodenal acidification on the effects of bombesin on gastric and pancreatic secretion and on blood levels of gastrin, secretin, and cholecystokinin (CCK) in six conscious dogs with chronic gastric and pancreatic fistulas. Duodenal acidification suppressed bombesin-stimulated gastric acid output (from 20.1 +/- 4.2 to 8.2 +/- 1.9 mEq/120 min) and gastrin release (from an integrated 2-hour output of 16.0 +/- 1.2 to 11.1 +/- 1.1 ng-min/ml). On the other hand, duodenal acidification augmented bombesin-stimulated secretion of pancreatic bicarbonate (from 0.75 +/- 0.12 to 7.81 +/- 2.0 mEq/120 min) and protein (from 0.57 +/- 0.10 to 1.00 +/- 0.18 gm/120 min). Blood levels of CCK (but not of secretin) were increased with bombesin alone, whereas blood levels of secretin (but not CCK) were increased by duodenal acidification alone. Bombesin plus duodenal acidification resulted in increase of both CCK and secretin. This increase of secretin may be responsible, in part, for suppression of both gastric acid output and gastrin release, as well as for increases in pancreatic secretion of bicarbonate and protein.

Animals↗
PubMed1980

Release of pancreatic polypeptide in humans by infusion of cholecystokinin.

Plasma levels of pancreatic polypeptide were measured after a test meal and after infusion of graded doses of 99% pure cholecystokinin in 6 healthy volunteers. Initial attempts at sterilization of 99% pure cholecystokinin resulted in complete inactivation. Successful sterilization was accomplished by filtration by using specially treated silver-coated filters. Biologic activity of sterilized material was confirmed with cholecystokinin bioassay, and plasma levels of sterilized cholecystokinin achieved by exogenous infusions were measured with a specific cholecystokinin radioimmunoassay. Significant increases in plasma levels of pancreatic polypeptide were found with a test meal and with infusions of 0.25 and 0.5 micrograms/kg-hr of 99% pure cholecystokinin. Integrated values of pancreatic polypeptide released by the low-dose and the high-dose infusions of 99% pure cholecystokinin were 59% and 50% of that obtained by food, respectively. Integrated levels of cholecystokinin after 45 min of infusion of 0.25 micrograms/kg-hr were equal to those after a standard meal. Cholecystokinin, therefore, is an effective humoral releaser of pancreatic polypeptide in humans and may play an important role in the intestinal phase of release of pancreatic polypeptide.

Adult↗
PubMed1979

Effect of parenteral L-amino acids on gastric secretion and serum gastrin in normal dogs and dogs with portacaval transposition.

The effect of intravenous infusion of L-amino acids (FreAmine II) on gastric secretion and on circulating levels of gastrin was studied in five gastric fistula dogs and three dogs with portacaval transposition. Significant increases in gastric acid secretion were found after infusions which delivered 2.0, 4.0, and 8.0 gm/hr of L-amino acids in five gastric fistula dogs. After portacaval transposition, administration of amino acid solutions via the hindleg (through the liver) resulted in a great fall in the acid secretory response. Gastrin levels were significantly elevated after 8.0 gm/hr of amino acids. After 2.0 and 4.0 gm/hr, there was a slight but insignificant increase in serum gastrin levels. Gastrin levels were unchanged after infusion of 8.0 gm/hr of L-amino acids through the liver. We conclude that L-amino acids given intravenously stimulate gastric acid secretion in a dose-dependent manner by a mechanism which does not involve gastrin. At the highest dosage of amino acids, some gastrin was released which might have stimulated acid output further.

Amino Acids↗
PubMed1979

[Effect of hypophysectomy on gastrin release and antral gastrin concentration].

Hypophysectomy resulted in a lower amount of basal serum gastrin. In hypophysectomized rats, there was a release of serum gastrin after food intake; however, the serum gastrin level was lower 30 min postprandially. The most important effect of hypophysectomy is absence of repletion of antral gastrin after an initial postcibarial depletion. We conclude that the immediate synthesis of antral gastrin after food intake is inhibited by hypophysectomy.

Animals↗
PubMed1979

Effect of vagal stimulation on pancreatic secretion and on blood levels of gastrin, cholecystokinin, secretin, vasoactive intestinal peptide, and somatostatin.

We investigated in dogs the effect of graded frequencies of electrical vagal stimulation (1.5, 3, 6, and 12 cps) on pancreatic exocrine secretion and on portal blood levels of gastrin, secretin, cholecystokinin (CCK), vasoactive intestinal peptide (VIP), and somatostatin (STS). Stimuli of all four frequencies, each with a duration of 5 minutes, were applied with a secretin background of 0.25 CU/kg-hr, and one stimulatory period of 12 cps was applied without a secretin background. With secretin, a significant, frequency-dependent increase of volume and of pancreatic protein secretion occurred from 3 to 12 cps. Gastrin values increased significantly at all frequencies. VIP and STS increased significantly with 3, 6, and 12 cps. Maximal responses for gastrin, VIP, and STS were observed with 6 cps. Peak values for gastrin and VIP were found during stimulation, whereas STS peaked after the end of the stimulatory period. The integrated responses of gastrin and STS showed significant correlation (P less than 0.01). The results suggest that vagally induced pancreatic response is only partially mediated by gastrin and perhaps VIP, and that endogenous gastrin may be one of the releasing factors for somatostatin. Plasma levels of CCK and secretin did not change after electrical stimulation, which provides direct evidence that their release is unlikely to be under vagal control, and that CCK does not mediate the protein secretion obtained after electrical stimulation of the vagus.

Animals↗