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Biomedical subjects

M M Wolfe

Publications and source records attributed to M M Wolfe.

99 records · Page 6Linked to original sources
PubMed1982

Portal and cephalic venous gastrin after peptone infusion in the alert dog.

A model was designed to permit sampling of portal venous blood in nonanesthetized dogs. Five mongrel dogs were prepared with indwelling portal venous catheters and gastric fistulas. After a minimum recovery period of 7 days, a 10 percent peptone meal was infused into the stomach. Portal and peripheral venous sera were obtained in the basal state and at various time points after intragastric peptone infusion. Serum gastrin concentrations were later measured by radioimmunoassay. Mean basal gastrin from portal and peripheral venous sera were 17 +/- 5 and 13 +/- 2 pg/ml, respectively. After peptone infusion, a biphasic gastrin response was observed. The first peak in portal venous serum occurred at 2 minutes, increasing to 49 +/- 20 pg/ml, while in the peripheral venous serum, the initial peak occurred at 4 minutes to 33 +/- 4 pg/ml. The second peak component occurred at 30 minutes in both circulations, increasing to 35 +/- 14 pg/ml in portal venous serum and to 29 +/- 8 pg/ml in peripheral venous serum. The results of this study (1) demonstrate that the release of gastrin after a peptone meal in the dog is prompt and biphasic, and (2) provide an effective method for obtaining simultaneous portal and peripheral venous blood for measurement of gastrointestinal peptides in alert, nonanesthesized dogs.

Animals↗
PubMed1982

Uptake of vasoactive intestinal peptide by rat liver.

We have investigated the uptake and degradation of vasoactive intestinal peptide (VIP) by rat livers. When liver was perfused with 125I-VIP, less than 20% of the radioactivity was recovered as intact peptide. 125I-VIp bound to specified high-affinity sites on isolated hepatocytes. Half-maximal inhibition of binding occurred at about 1 nM unlabeled VIP. Cell-bound 125I-VIP was degraded to low-molecular-weight products. The percent of 125I-VIP that was bound and degraded was approximately the same at both extremes of the range of VIP concentrations (25-250 pg/ml) reported in portal vein plasma. The lysosomotropic agent chloroquine inhibited 125I-VIP degradation and led to the accumulation of cell-bound 125I-VIP. We conclude that a) most of the VIP secreted from the gastrointestinal tract into portal blood is removed during its passage through the liver, b) VIP binds to specific high-affinity sites on hepatocytes and is probably internalized and degraded by lysosomes, and c) uptake of VIP by liver may serve to prevent the peptide from exerting deleterious systemic effects.

Animals↗
PubMed1982

Release of gastric inhibitory peptide following a peptone meal in the dog.

Release of gastric inhibitory peptide into the circulation after peptone ingestion has not been demonstrated previously. In the present studies, 5 alert dogs with indwelling polyethylene portal venous catheters and gastric fistulas were studied. A meal of 10% peptone in 150 ml 0.9% NaCl, pH 7 was infused through the gastric fistula into the stomach. Gastric inhibitory peptide was measured by a specific and sensitive radioimmunoassay in sera obtained simultaneously from portal and cephalic veins before and at 1, 4, 8, 15, 30, 60, and 90 min after peptone infusion. Cephalic venous serum insulin and glucose concentrations were measured at the same time points. Mean basal portal and cephalic vein serum gastric inhibitory peptide concentrations were 136 +/- 22 and 34 +/- 10 (SEM) pg/ml, respectively. After infusion of the peptone meal, immediate increases in serum gastric inhibitory peptide levels were noted in both portal and peripheral circulation, with a peak of 597 +/- 151 pg/ml (p less than 0.02) at 8 min in portal venous serum and 323 +/- 95 pg/ml (p less than 0.05) at 15 min in cephalic venous serum. No significant increases in peripheral venous serum insulin concentration were detected throughout the entire collection period, whereas peripheral venous serum glucose levels increased slightly from a fasting level of 56 +/- 5 mg/dl to 72 +/- 5 mg/dl (p less than 0.05) at 90 min. The mean half-time of disappearance of intravenously administered gastric inhibitory peptide was found to be 7.6 +/- 1.5 (SEM) min. Results of these studies demonstrate prompt stimulation of gastric inhibitory peptide response to peptone, with peak serum gastric inhibitory peptide concentrations which are higher and occur earlier in portal than in peripheral blood. Gastric inhibitory peptide was found to have a brief half-time of disappearance, similar to that of other structurally related gastrointestinal peptides.

Animals↗
PubMed1981

Effect of antrectomy on the nervous phase of gastric secretion in the dog.

A method is described for complete isolation of the stomach in the dog with vagal innervation intact. This involves esophagostomy, double mucosal closure of the pylorus and a Maydl gastric fistula combined with gastrojejunostomy. The latter is occluded during periods of study. In this preparation the responses to sham feeding and to insulin-induced hypoglycemia were reduced approximately 10-fold, reiterating the significant synergistic effect of gastrin on vagal stimulation of the parietal cell mass. However, significant acid secretion could still be induced in this preparation by both sham feeding and insulin-induced hypoglycemia.

Animals↗