Effect of vagotomy on the feedback inhibition of pancreatic secretion

Chronic experiments on fistulized dogs showed that the pancreatic secretion stimulated by intraduodenal administration of acidified hydrolysine was depressed after bilateral supradiaphragmatic truncal vagotomy, and that the inhibitory influence of exogenous pancreatic enzymes on pancreatic secretion disappeared on postoperative days 10–16. Subsequently, the feedback inhibition of pancreatic secretion was slowly restored, but even 45 days after vagotomy it was still weaker than in intact dogs. It is concluded that the feedback inhibition of pancreatic secretion is centrally controlled from the duodenum via the vagus nerves. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 119, N ^o 5, pp. 465–469, May, 1995 Presented by K. V. Sudakov, Member of the Russian Academy of Medical Sciences     

Effect of truncal vagotomy on the state of pyloric muciferous cells

The pyloric glands and muciferous superficial cells of the pyloric mucosal membrane have been studied in 62 patients with complicated forms of duodenal ulcer--preoperatively, 2--4 weeks, 6--12 months following truncal vagotomy with drainaged stomach. The light transmission and scanning electron microscopy and stereometry, were used as well as the determination of mucosal production and intragastric pHmetry. It is shown that vagotomy leads to a decrease of inflammatory changes without an essential influence on the pyloric gland size. Ultrastructure of muciferous cells gives evidence of their significant possibilities for mucus production, although the production of gastric mucosal components decreases postoperatively. Apart from this essential decrease of the main and parietal cell size and their secretory activity was noted. This provides an adequate level of acid-neutralizing gastric function following vagotomy.     

Effect of substance P and its C-terminal hexapeptide on gastric and pancreatic secretion in the dog

In five dogs with gastric fistulas, Heidenhain pouches, and pancreatic fistulas, the effects of substance P (SP) and its C-terminal hexapeptide (SP6-11) on gastric acid and pancreatic secretions were determined under basal conditions and in response to secretory stimulation. SP or SP6-11 infused alone in graded doses (0.25-2.0 nmol.kg-1.h-1) caused a slight but significant increase in pancreatic secretions in fasted dogs, but, when given during the secretory stimulation, they caused significant inhibition of these secretions. They reduced gastric acid response to pentagastrin and peptone meal without affecting the serum gastrin level. They caused dose-dependent inhibition of secretin-induced pancreatic bicarbonate secretion and suppressed the pancreatic protein response to caerulein, feeding, and duodenal acidification. SP6-11 was equipotent on a molar basis with SP in the inhibition of gastric or pancreatic secretion, indicating that the C-terminal portion of SP exhibits a full spectrum of the biological action of the intact molecule. The inhibitory effects of SP and SP6-11 on the stomach and pancreas were observed at a dose range that was without any significant influence on the blood pressure, indicating that they are not caused by the interference of the blood flow to the pancreas.     

Pancreatic and intestinal growth-promoting effect of truncal vagotomy in the rat

The effect of chronic subdiaphragmatic truncal vagotomy was investigated on body weight gain, food intake pattern, and also on intestinal and pancreatic growth, in adult rats. Two sham-operated groups, the one fed ad libitum, the other pair-fed with the vagotomized rats, served as controls. Body weight of vagotomized rats decreased in the first 5 postoperative days, due to hypophagia. Then, body weight increased as food intake reached the presurgery level. The rats were killed after 34 days of vagotomy. A moderate pancreatic and intestinal hypertrophy was observed in the vagotomized rats, while the tissue weight of and the DNA and protein contents in the colon and the oxyntic and antral areas of the stomach did not change compared to controls. The mechanism of the intestinal and pancreatic hypertrophy is unknown; several humoral and nervous factors may be involved in it.     

Long-term changes in the rat gastric mucosa after truncal vagotomy and pyloroplasty

In 40 male mature albino Wistar rats histological changes of gastric mucosa were analyzed, parietal and chief cells were counted and gastric juice pH was determined 120, 240 and 365 days after truncal vagotomy and pyloroplasty. In all the groups gastric mucosa was attenuated and morphological signs of preatrophic gastritis (decline in parietal cells number, a certain mucoidization of fundal glands without changes in surface epithelium, alteration of mucosal lamina propria) were present. On the background of atrophic changes compensatory and adaptive processes (increase of mitotic activity of epitheliocytes--precursors of differentiating cells, normalization of parietal cells differentiation along the stem line, i.e. of ratio of differentiating, mature functioning and degenerating cell forms) were noted, that lead to repair of histo-structure and function on the whole, although at a lower level. Following long-term intervals after vagotomy glandular gastric epithelium acquires its histo-typical form with parietal secretory activity decreased to some extent.     

A vasopressin-induced decrease in pancreatic blood flow and in pancreatic exocrine secretion in the anesthetized dog

Vasopressin decreases blood flow as well as secretory flow in the pancreas. The question raised was whether the blood flow decrease is the determinant of the decrease in secretion or quite the reverse. In pentobarbital anesthetized dogs, secretory flow was first increased to a steady level by infusion of secretin. At this steady state, O₂ consumption and O₂ extraction were increased, while blood flow remained at the control level, indicating an increase in the area available for exchange i.e. an increase in capillary density. At increasing doses of vasopressin, secretory flow decreased, arterial flow decreased, and O₂ extraction increased, while O₂ consumption decreased and venous-arterial CO₂ concentration difference was not changed. At the same time CO₂ transport decreased, CO₂ concentration in the secretion was unchanged and CO₂ output in the secretion was decreased. The decrease in blood flow was always seen about 25 s before the decrease in secretory flow, strongly suggesting that the decrease in blood flow induced the decrease in secretory flow. A higher dose of vasopressin was required to decrease the O₂ consumption (i.e. this effect was less sensitive) than to increase O₂ extraction. The decrease in secretory flow and the decrease in blood flow showed an intermediate sensitivity. So O₂ consumption seems to be preserved at a high level by the increase in O₂ extraction. It is concluded that the vasopressin-induced decrease in blood flow is the determinant of the decrease in secretory flow. This phenomenon is discussed in terms of the model for metabolic control of tissue oxygenation.     

Effect of motilin on pancreatic secretion

Summary Motilin and secretin were compared in regard to their effects on pancreatic bicarbonate and protein secretion in conscious dogs provided with chronic pancreatic fistulas. Dose-response analysis showed that maximal bicarbonate response to motilin was about 5% of that to secretin and maximal protein response was about 35% of that to caerulein. The interaction of these two peptides showed that motilin is a potent inhibitor of secretin-induced bicarbonate secretion. Since motilin is released by duodenal alkalinization and inhibits pancreatic bicarbonate secretion, it is possible that this peptide is involved in the feedback mechanism of inhibition of pancreatic secretion by alkaline pancreatic juice present in the duodenum.