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Biomedical subjects

S Andersson

Publications and source records attributed to S Andersson.

At least 289 records · Page 16Linked to original sources
PubMed1980

Inhibition of acid secretion from vagally innervated and denervated gastric pouches by (Gln4)-neurotensin.

In dogs with innervated fundic pouches an intravenous infusion of (Gln4)-neurotensin, 60 pmol X kg-1 X min-1, reduced the pentagastrin-stimulated acid secretion to 40% of the control secretory rate. After vagal denervation of the fundic pouches the same dose of (Gln4)-neurotensin did not significantly change the secretion. These findings suggest that (Gln4)-neurotensin does not act directly on parietal cells but inhibits acid secretion at a presynaptic level.

Animals↗
PubMed1979

Glucose memory of pancreatic B and A2 cells: evidence for common time-dependent actions of glucose on insulin and glucagon secretion in the perfused rat pancreas.

The influence of previous exposure to glucose on the subsequent B- and A(2)-cell secretory responses to arginine was investigated in the perfused pancreas of the rat. Arginine (8 mM) was administered in two brief (9 min) pulses separated by a period of 66 min. In pancreata from 18-h-fasted animals the two pulses of arginine elicited biphasic glucagon secretory responses, while stimulation of insulin release was barely detectable. When 27.7 mM glucose was administered for 30 min during the intervening period up to 20 min before the second pulse of arginine, the glucagon response to arginine was diminished by 55% while the insulin release was markedly increased in comparison with the first pulse. 8.3 mM glucose, when administered before the second pulse of arginine, exerted effects that were smaller but otherwise similar to those of 27.7 mM glucose.The inclusion of 3.9 mM glucose during the stimulation periods with arginine decreased the glucagon and greatly increased the insulin secretory response. Under these conditions, previous exposure to 27.7 mM glucose inhibited the glucagon and enhanced the insulin response to the second stimulatory pulse of arginine to the same relative degree as when arginine was administered alone. Diazoxide (2 mM), when administered together with 27.7 mM glucose, almost completely inhibited insulin release induced by the presence of glucose, yet did not influence the modulation exerted by glucose on the subsequent insulin and glucagon secretory response to arginine. Conversely, these effects of the glucose pulse could not be reproduced by 1 mug/ml of porcine insulin. Previous exposure to glyceraldehyde (10 mM) mimicked the glucose effects.Also, in pancreata from fed rats, previous exposure to 27.7 mM glucose markedly inhibited subsequent arginine-induced glucagon secretion while the concomittant insulin response was enhanced.IT IS CONCLUDED THAT: (a) both A(2)- and B-cell responsiveness is modulated by a previous exposure to glucose which produces opposite effects in the two cell types, (b) this action of glucose does not depend on its insulin-releasing capacity, and (c) instead, a "memory" of glucose is induced as a consequence of the metabolism of the sugar in the A(2) and B cells.

Animals↗
PubMed1977

Inhibition of gastric and intestinal motor activity in dogs by (Gln4) neurotensin.

The action of (Gln4)-neurotensin was studied on the spontaneous motor activity in isolated canine fundic, antral and intestinal pouches. All pouches had been prepared more than 6 months prior to the experiments. Spontaneous motor activity was recorded for at least 1 h before the Gln4)-neurotensin was infused i.v. for 30 min in doses ranging between 6.3 and 100 ng X kg-1 X min-1. In the vagally denervated fundic pouches (Gln4)-neurotensin inhibted motor activity in doses above 25 ng X kg-1 X min-1. The vagally innervated antral pouches were more sentitive than the vagally denervated fundic pouches to the action of (Gln4)-neurotensin. Thus motor inhibition was induced by doses as low as 6.3 ng X kg-1 X min-1. The effect of (Gln4)-neurotensin on motor activity in intestinal pouches was inconsistent. Inhibition was seen in 1 out of 7 expts. The present results show that the gastric motor activity is the most sensitive function to (Gln4)-neurotensin so far studied.

Animals↗
PubMed1977

Effect of resection of antrum and duodenal bulb on sham-feeding-induced inhibition of canine gastric secretion.

In dogs with Heidenhain pouches and oesophageal and gastric fistulae, sham feeding inhibited pentagastrin-stimulated Heidenhain pouch acid output. Resection of the antrum and the duodenalbulb reduced oin stomach was diverted through the gastric cannula. The present results are conid secretion at least partly by inducing a vagal release of an inhibitory hormone. The results suggest that this hormone is released from the antrum and the duodenal bulb.

Animals↗
PubMed1976

[Non-resecting surgery for gastroduodenal ulcer. I. Pathophysiological principles (author's transl)].

Selective proximal vagotomy with pyloroplasty is a method which permits ulcers to be operated on with less morphological and pathophysiological disturbances than is possible with any other method. After ingestion, a reactive yet reduced acid secretion is still possible through the gastrin stimulus. The retained vagal antral release of gastrin seems to be without importance to the denervated delomorphous cells. Side effects of this type of vagotomy are small. The disturbances of motility and evacuation which also occur here can easily be corrected by an additional pyloroplasty suitable in shape and function.

Animals↗
PubMed1976

Gastric secretory and motor inhibition induced by certain methyl analogues of prostaglandin E2 in healthy male volunteers and in patients with duodenal ulcer disease.

The present investigation shows that the 15(S)-15-methyl and 16,16-dimethyl analogues of PGE2 given orally are potent inhibitors of gastric acid secretion. The inhibition of acid output is mainly due to a reduction in volume output. The effect on acid secretion was shown to be less pronounced in a group of duodenal ulcer patients than among healthy volunteers. Only the 15-methyl analogue gave any significant secretory inhibition following intestinal administration. The results from the experiments in dogs indicate that a local action on the oxyntic glands could be the main reason for secretory inhibition following oral administration. The results from the studies on motor activity show that the prostaglandins inhibit both antral and duodenal pressure activity. However, with our experimental design, only with doses exceeding those required for secretory inhibition.

Animals↗
PubMed1975

Gastric secretory inhibition by two 16-methylated analogs of prostaglandin E2 given intragastrically to patients with duodenal ulcer disease.

The effects of two methylated analogs of prostaglandin E2 (PGE2), namely 16,16-dimethyl PGE2 and its methyl ester, on gastric acid and pepsin secretion have been studied in 5 ulcer patients. Both analogs produced significant inhibition of acid secretion in a dose-dependent fashion, but the effect was less pronounced than the inhibition found in a group of healthy volunteers, and it was necessary to give 140 mug of each analog to reach about the ED50. The mean values of pepsin output and pepsin concentration were decreased following administration of PGE2, but the individual results varied.

Adult↗
PubMed1975

Effect of two methylated prostaglandin E2 analogs on gastroduodenal pressure in man.

The effect of two methylated analogs of prostaglandin E2 (PGE2), namely 16, 16-dimethyl PGE2 and 15 (S)-15-methyl PGE2 methyl ester, on gastroduodenal motility has been studied in healthy male volunteers. Oral administration of 140 mug of the 16-alkylated analog produced a significant decrease in motor activity in both the gastric antrum and the duodenum. 80 mug had no detectable effect on pressure. However, 80 mug of the 15-methylated analog administered directly into the duodenum caused an almost immidiated inhibition of the duodenal motor activity. In view of previous findings on the inhibitory action of these two analogs on gastric acid secretion, it seems as if the gastrointestinal smooth muscles are less sensitive to the action of the analogs than are the oxyntic glands.

Administration, Oral↗