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U Grötzinger

Publications and source records attributed to U Grötzinger.

30 records · Page 2Linked to original sources

[Addition of albumin to solutions of cholecystokinin (CCK)--effect on pancreatic secretion, plasma CCK level and release of pancreatic polypeptide (PP)].

Dissolving basic peptides such as insulin, secretin, and somatostatin in albumin-containing solutions increases the biologic potency. As CCK-33 also constitutes a basic peptide, it should have similar qualities. In four conscious dogs with chronic gastric and pancreatic Thomas fistulas, we studied the effect of CCK-33 solutions with and without addition of albumin on pancreatic secretin, plasma PP concentration, CCK-like immunoreactivity in plasma and infusion lines. The response of pancreatic protein output (mg/15 min) to increasing doses of 99% pure CCK-33 (0.5; 1; 2; 4 IDU/kg/h) was significantly higher (p less than 0.05) when CCK was dissolved in 0.154 M NaCl with albumin than in NaCl alone. These results were confirmed by measuring plasma CCK-immunoreactivity by CCK-RIA and CCK-immunoreactivity in samples from tips of infusion lines by gastrin-RIA. CCK evoked PP release at increasing doses of CCK-33, which was significantly (p less than 0.05) higher when CCK was dissolved in an albumin-containing solution. There was a significant (p less than 0.02) correlation between plasma PP concentration and pancreatic protein output. Our study shows addition of albumin to solutions of CCK-33 to cause an increase of CCK-33 activity, probably by preventing adsorption of the peptide to glass and plastic surfaces. This is valid for its effect on pancreatic protein secretion as well as PP release.

Albumins↗

Vagovagal stimulation of pancreatic-polypeptide secretion by graded distention of the gastric fundus and antrum in man.

Previous studies have shown that pancreatic polypeptide (PP) secretion is regulated by efferent, vagal stimulation. In the present study the afferent part of a vagovagal pathway has been investigated in two different ways: (I) Graded fundic distention: in 8 patients with duodenal ulcer ballon distention with 150 ml of the fundus and the body of the stomach increased PP concentrations in plasma from 19 (17--26) to 41 (35--48) pmol/l, median and interquartile range. Distention by 300 and 600 ml did not further increase PP concentrations. After denervation of the fundus by proximal gastric vagotomy, no increase in PP levels was observed during distention with 50 and 300 ml whereas distention by 600 ml was followed by a small increase. (II) Graded antral distention: balloon distention with 50, 100 and 150 ml of the antrum increased plasma PP concentrations in 7 healthy subjects and 14 duodenal ulcer patients. Maximal PP response was achieved by distention with 100 ml, healthy subjects: from 14 (12--23) to 40 (26--44) pmol/l, and duodenal ulcer patients: from 25 (13--38) to 47 (22--63) pmol/l, median and interquartile range. It is concluded that a gastropancreatic reflex stimulating PP secretion through a long vagovagal pathway is present in man, and that this mechanism probably is involved in the initial PP response during a meal.

Adult↗

Evidence for a defective inhibition of pentagastrin-stimulated gastric acid secretion by antral distension in the duodenal ulcer patient.

Graded antrum distension by 50-, 100-, and 150-ml balloon volumes significantly stimulated gastric acid secretion in 6 duodenal ulcer patients, but had no stimulatory effect in 6 healthy subjects. Antrum distension by 150-ml balloon volume had no effect on the acid response to submaximal stimulation by a continuous intravenous infusion of pentagastrin in the duodenal ulcer patients, but significantly inhibited this response in the healthy subjects. The inhibition by antrum distension in the healthy subjects amounted to 20%. The results suggest that antrum distension elicits stimulatory as well as inhibitory mechanisms in man with inhibition of acid secretion predominating in healthy subjects and stimulation of acid secretion predominating in duodenal ulcer patients. The mechanism of inhibition is unknown.

Adult↗

Effect of fundic distension on gastric acid secretion in man.

The effect of distension of the fundus and body of the stomach on gastric acid secretion was studied in 26 patients with duodenal ulcer and six healthy subjects. Graded distension produced by inflating a rubber balloon to volumes of 150, 300, and 600 ml resulted in significant sequential increments of acid output. The secretory response outlasted stimulation by at least one hour. In both groups of subjects, the highest acid output obtainable with fundic distension amounted to just above 50% of the maximum secretory response evoked by intravenous infusion of pentagastrin. A significant correlation was found between the peak secretory rates observed during fundic distension and after pentagastrin stimulation. It is concluded that distension of the oxyntic gland area in man is a potent stimulus for gastric secretion of acid and that patients with duodenal ulcer are no more sensitive to this stimulus than healthy subjects.

Adult↗

Effect of atropine and proximal gastric vagotomy on the acid response to fundic distension in man.

In four healthy subjects and in 12 patients with duodenal ulcer (DU), graded balloon distension of the gastric fundus and body caused increments in acid output related to the distension volumes. The mean peak distension response amounted to about 50% of the mean peak acid output (PAOpg) evoked by intravenous infusion of pentagastrin in a dose of 300 microng/h, eliciting maximum observed secretory response. During distension with the largest balloon volume, 1-0 mg atropine injected intravenously significantly depressed the acid secretory rate, the median inhibition amounting to about 80%. In two patients with DU, 2-5 mg atropine completely abolished acid secretion during fundic distension. In nine subjects with DU, complete proximal gastric vagotomy profoundly depressed the secretory responses to graded fundic distension, eliminating the acid response to the smallest balloon volume used. A slight, but significant, response to the largest distension volume persisted after complete vagotomy. Incomplete proxomal gastric vagotomy was found to reduce only moderately the distension responses in five patients, and the peak acid response to fundic distension as related to PAOpg remained unchanged. In conclusion, distension of the gastric fundus and body in man stimulates acid secretion by means of an atropine-sensitive, presumably cholinergic, reflex mechanism and the findings after vagotomy are in agreement with the concept that this reflex mechanism is conveyed by both short intramural and long vagovagal pathways.

Adult↗

Effects of fundic distention on pentagastrin-stimulated gastric acid secretion in man.

The acid secretory effect of combined stimulation with balloon distention of the fundus and body of the stomach and intravenous infusion of pentagastrin has been studied in patients with duodenal ulcer (DU) and in healthy subjects. In 8 nonoperated DU subjects and in 5 DU patients subjected to proximal gastric vagotomy, low grade fundic distention moderately enhanced the acid output evoked by a threshold dose of pentagastrin. Fundic distention with a baloon volume eliciting a maximal acid response to distention either left unchanged or suppressed the maximal acid secretory rate produced by pentagastrin in 7 nonoperated and 6 vagotomized DU patients and in 5 healthy subjects. The heterogeneous secretory effects of maximal stimulus combination suggest that fundic distention has a complex action on acid secretion eliciting a hitherto unknown inhibitory effect as well as a cholinergic activation of the parietal cell area. This complex action may explain the failure of fundic distention to augment markedly the action of pentagastrin in the present study.

Adult↗

Is there an oxyntopyloric reflex for release of gastrin in man?

Plasma gastrin concentrations and gastric acid output were measured during graded balloon distention of the gastric fundus and body in 20 patients with duodenal ulcer. Acid output rose stepwise with increasing distention volumes but plasma gastrin remained unchanged. During intragastric neutralization in 5 of these subjects, fundic distention did not elicit a significant rise in plasma gastrin, whereas the acid response was similar to that observed in the control study when the gastric contents were acid. In 8 of the 20 patients, proximal gastric vagotomy profoundly suppressed the acid response to fundic distention. Basal plasma gastrin concentrations were elevated after vagotomy but were unchanged during graded fundic distention. The results suggest that neural reflex activation of the oxyntic glands is the main mechanism by which fundic distention stimulates acid secretion in man. The failure of fundic distention to release gastrin does not, however, completely rule out the existence of an oxyntopyloric distention reflex for gastrin release in man. Fundic distention in man seems to both stimulate acid secretion and induce an inhibitory mechanism acting on acid secretion. This inhibitory mechanism may, purely speculatively, also mask the effect of an oxyntopyloric reflex for gastrin release. The present study and earlier work suggest that in man distention of the stomach is a poor stimulus for release of gastrin, regardless of whether the pyloric or the oxyntic gland area, or both, are distended.

Adult↗