Vein Somatostatin-like Immunoreactivity Research Articles

Effect of β-Casomorphins on Somatostatin Release in Dogs*

In the present study, the effects of orally administered beta-casomorphins (beta-CM) and met-enkephalin on postprandial plasma somatostatin-like immunoreactivity (SLI) were assessed in conscious dogs. The intragastric instillation of a liver extract-sucrose test meal containing 12 mg beta-CM or 10 mg met-enkephalin, respectively, augmented the postprandial rise of peripheral vein plasma SLI levels significantly. This effect was inhibited by the additional administration of the specific opiate-receptor antagonist, naloxone. When liver extract-sucrose was dissolved in fresh bovine milk the increase of plasma SLI levels was significantly greater than liver extract-sucrose dissolved in water. This milk-induced augmentation of SLI levels was also reduced by naloxone. Since these opiate-active compounds have an influence upon insulin release when given iv, the effect of beta-CM-7, beta-CM-5, beta-CM-4 beta-CM-4-amide, and met-enkephalin on SLI levels was assessed during their iv infusion at a rate of 1 nmol/kg . h during an iv background infusion of a glucose-amino acid mixture. The infusion of beta-CM-5 elicited a stimulation of peripheral vein SLI levels, whereas the infusion of met-enkephalin resulted in a significant decrease of SLI levels. beta-CM-7, beta-CM-4, and beta-CM-4-amide had no effect on plasma SLI levels at the dose employed. The present data demonstrate that in dogs the ingestion of opiate-active peptide stimulates postprandial SLI release, indicating that nutrient-contained opiate-active material (exorphins) might participate in the regulation of postprandial gastrointestinal endocrine function.

Role of histamine H 2-receptors in gastric and pancreatic release of somatostatin-like immunoreactivity during the gastric phase of a meal

The present study was designed to determine the role of H 2-receptors in the postprandial release of somatostatin-like immunoreactivity (SLI) from the gastric fundus and antrum and from the pancreas. In dogs subjected to laparotomy, the pylorus was bisected and a gastric fistula was created, following which 250 ml 20% liver extract (LE) at pH 7 or 2 were instilled intragastrically. In the fundic vein the incremental SLI rise in response to LE at pH 7 was 2423 ± 540 pg/ml during a control infusion of saline and 4780 ± 863 pg/ml during the infusion of cimetidine (1 mg/kg per h) ( P < 0.05). In the antral vein the incremental SLI in response to LE at pH 7 was 2182 ± 530 pg/ml during the saline control but did not rise significantly during cimetidine infusion. In the pancreatic vein the incremental SLI level after LE at pH 7 was 1953 ± 358 pg/ml in the control experiments and 4430 ± 1024 pg/ml during cimetidine infusion ( P < 0.025). The incremental inferior vena cava SLI level was approximately 925 pg/ml in both groups (not significant). The instillation of LE at pH 2 during the saline control lowered fundic vein SLI by 500 pg/ml; this decline was abolished during cimetidine infusion. In the antral vein the incremental SLI level of 15 750 ± 2514 pg/ml during saline was lowered to only 6728 ± 2257 pg/ml during cimetidine (ifP < 0.025). After LE at pH 2 the incremental pancreatic vein SLI level of if5641 ± to be one regulatory component in the modulation of gastric acid secretion and gastrin release [21,26] during the gastric phase of a meal. The possible involvement of H 2-receptors in this regulatory system is schematized in Fig. 7. Pancreatic SLI release is also influenced by H 2-receptors but this appears to depend on the intragastric pH; stimulation of the receptors appears to lower the pancreatic SLI response to neutral protein and raise the response to acidified protein. If these effects are due to stimulation of gastric and/or pancreatic H 2-receptors can not be determined from the present data. These findings, in conjunction with previous studies [21–25], reveal a highly complex regulatory system for somatostin release during the gastric phase of meal, and indicate that, in addition to the influence of muscarinic-cholinergic [23], adrenergic mechanisms [24] and prostaglandins [25], reveal a histaminergic influence must now be recognized.

Release of pancreatic and gastric somatostatin-like immunoreactivity in response to the octapeptide of cholecystokinin, secretin gastric inhibitory polypeptide, and gastrin-17 in dogs.

The effects of the gastrointestinal hormones cholecystokinin- octapeptide (CCK-OP), secretin, gastric inhibitory polypeptide (GIP), and gastrin-17-I, infused at approximately their physiological rate, upon the release of pancreatic and gastric somatostatin-like immunoreactivity (SLI) were studied in dogs. In anesthetized dogs, CCK-OP, administered iv at a rate of 0.5 μg/kg·h, elicited increases in plasma levels of SLI of approximately 60 pg/ml in the inferior vena cava, 300 pg/ml in the pancreatic vein, 280 pg/ml in the fundic vein, and 300 pg/ml in the antral vein. During the infusion of secretin at a rate of 0.1 C.U./kg·h, inferior vena caval and gastric vein SLI levels did not change, although pancreatic vein SLI rose by 160 pg/ml with secretin administered at a supraphysiological rate of 1.0 C.U./kg·h, inferior vena caval SLI levels rose 30 pg/ml, pancreatic venous SLI levels rose 240 pg/ml, and fundic and antral venous SLI levels rose 120 and 160 pg/ml, respectively. GIP, infused at a rate of 1.0 μg/...

Effect of exogenous and endogenous prostaglandin E upon gastric endocrine function in dogs.

The effects of prostaglandin E2 (PGE2) and indomethacin- induced endogenous PGE deficiency upon basal and postprandial release of gastric somatostatin-like immunoreactivity (SLI), glucagon, and gastrin during the gastric phase of a meal were determined in anesthetized, laparotomized dogs. The infusion of PGE2 (1 μg/kg- min) elicited a sustained rise in antral vein and inferior vena cava plasma SLI levels and a transient SLI rise in the fundic vein. Antral vein and inferior vena cava gastrin decreased significantly during PGE2 infusion, while fundic vein and inferior vena cava glucagon rose significantly. Indomethacin infusion (2 mg/kg-h) elicited a significant decrease in basal SLI levels in the fundic and antral veins and in the inferior vena cava plasma and a significant increase in basal antral vein gastrin levels, but no change in basal inferior vena cava gastrin or in basal fundic vein or inferior vena cava glucagon levels. The effects of PGE2 infusion upon postprandial SLI, gastrin, and glucagon var...

Pancreatic and gastric release of somatostatinlike immunoreactivity during intestinal phase of a meal.

The present study was designed to examine pancreatic and gastric D-cell function during the intestinal phase of a liver meal. The intraduodenal instillation of a 20% liver meal (5 ml/min) elicited a significant rise in the plasma levels of somatostatinlike immunoreactivity (SLI) in the pancreatic vein and inferior vena cava, together with the rise in glucagon and insulin levels. The rise in pancreatic vein SLI was not reduced after truncal vagotomy or during atropine infusion. In the stomach, the intestinal liver meal elicited a significant rise in antral but not fundic vein SLI levels. The rise in antral vein SLI was augmented after truncal vagotomy and abolished during atropine infusion, as was the rise in inferior vena caval SLI. In contrast to the protein meal, intravenous infusion of an amino acid mixture elicited a rise in pancreatic vein SLI but not antral or fundic vein SLI. It is concluded that during the intestinal phase of a protein meal, pancreatic and antral but not fundic SLI release is stimulated. The effects of truncal vagotomy and atropine infusion on these responses suggest a close interaction between the vagus and muscarinic cholinergic mechanisms and the D cells of the stomach and pancreas.

Plasma somatostatin-like immunoreactivity in depancreatized dogs.

The present study was designed to determine the D cell response to ingested nutrients in totally depancreatized dogs. Basal levels of somatostatin-like immunoreactivity (SLI) averaged 135 ± 12 pg/ml in 7 depancreatized dogs and 146 ± 10 pg/ml in 30 controls (P = NS). In 7 conscious depancreatized dogs, an intragastric casein hydrolysate load elicited a small but significant rise of 20 pg/ml in peripheral venous plasma SLI levels during the first 60 min (P < 0.02); the incremental SLI (sum of the increments) during this period was 103 ±31 pg/ml, significantly less than the 278 ± 60 pg/ml in the normal control dogs (P < 0.05). In contrast to normal dogs, SLI did not rise in the depancreatized dogs in response to a fat-rich meat meal. After a liver meal, SLI levels rose by 30–40 pg/ml (P = NS) compared to the 80 pg/ml rise in the normal dogs. Gastric vein SLI levels were measured during laparotomy in six depancreatized and five control dogs after an intragastric load of casein hydrolysate. Antral vein SLI le...

Gastric and pancreatic release of somatostatin-like immunoreactivity during the gastric phase of a meal: effects of truncal vagotomy and atropine in the anesthetized dog.

The postprandial release of gastric and pancreatic somatostatin-like immunoreactivity (SLI) was examined in anesthetized dogs during the gastric phase of a meal, and the role of vagal and atropine-sensitive mechanisms in the responses was assessed. The intragastric instillation of liver extract at pH 7 elicited a significant rise in antral vein SLI (∼300 pg/ml) and gastrin concentration. After truncal vagotomy, both baseline and postprandial antral vein SLI and gastrin concentration increased significantly compared with the control group. The infusion of atropine (100 μg/kg/h) abolished the postprandial rise in antral vein SLI but not in gastrin. The liver meal at pH 2 elicited a sustained sixfold greater rise of antral SLI (∼2000 pg/ml) than that at pH 7, while gastrin concentrations did not rise significantly. The latter antral SLI response was not influenced by truncal vagotomy, but atropine infusion reduced it by about 50%. In response to the meal at pH 7, fundic vein SLI concentrations rose by about 300 pg/ml. The rise was augmented slightly by truncal vagotomy but was abolished completely by atropine infusion. In response to the meal at pH 2, fundic SLI decreased sharply below baseline levels. The response was not altered significantly by vagotomy, but was reversed completely by atropine infusion, during which fundic vein SLI concentrations rose significantly. Pancreatic vein SLI concentrations rose by about 350 pg/ml in response to the gastric meal at pH 7. That rise was not altered significantly by vagotomy but was abolished by atropine infusion. In response to the meal at pH 2, pancreatic SLI concentrations rose by about 1000 pg/ml above baseline, significantly greater than the response to the meal at pH 7. The pancreatic vein SLI response to the meal at pH 2 was not altered by vagotomy. It was reduced considerably by atropine infusion. It is concluded that SLI is released from the antrum, fundus, and pancreas during the gastric phase of a meal and that these responses are modified by acidification of the intragastric contents and by truncal vagotomy and atropine infusion. The greatly augmented release of antral SLI in response to the acidified meal raises the possibility of a role for somatostatin in acid-induced suppression of gastrin release.

Pancreatic and Gastric D Cell Function in Hypophysectomized Dogs*

The present study was designed to examine the effect of hypophysectomy upon gastric and pancreatic D cell function by determining the concentration of somatostatin-like immunoreactivity (SLI) in the venous effluents of the pancreas and stomach in response to an intragastric liver meal and acid load. In five sham-hypophysectomized (sham-hypox) control dogs, mean inferior vena cava SLI levels increased by 100 pg/ml above baseline in response to the liver meal and rose by an additional 450 pg/ml after the intragastric acid load. In the four hypophysectomized (hypox) dogs, mean inferior vena cava SLI levels did not differ significantly from the controls either before or after the liver meal, but decreased below baseline levels in response to the acid load, differing significantly from the values of the sham-hypox dogs. Pancreatic vein SLI levels of the sham-hypox dogs rose significantly by 600 pg/ml in response to the protein meal and increased further by 1000 pg/ml after the acid load. In the hypox group, pa...

Release of Gastric Somatostatin-Like Immunoreactivity During Acidification of the Duodenal Bulb

This study was designed to determine if gastric somatostatin is released during the acidification of the duodenal bulb or distal duodenum. A proximal duodenal pouch was per f used with HCl in normal laparotomized anesthetized dogs during an intravenous infusion of saline, pentagastrin (5 µg/kg/hr), or histamine (20 µg/kg/hr). Bulb acidification during i.v. saline was accompanied by a slight increase in antral vein somatostatin-like immunoreactivity (SLI), but no change in fundic vein SLI or inferior vena caval SLI levels occurred. Acidification of the bulb during i.v. pentagastrin elicited an increase in fundic vein SLI from a baseline level of 593 ± 205 pg/ml to a peak level of 1,554 ± 510 pg/ml (P

Pancreatic and gastric somatostatin release in response to intragastric and intraduodenal nutrients and HCl in the dog.

The effects of the instillation of glucose, fat, casein hydrolysate, and HCl into the gastrointestinal tract upon plasma levels of somatostatin-like immunoreactivity (SLI) in the venous effluent of the pancreas, fundus and antrum of the stomach, and in the inferior vena cava (IVC) were determined in normal laparotomized dogs. Fasting SLI levels in the effluent plasma from these sites were significantly greater than IVC levels. The intragastric administration of glucose elicited a prompt and significant rise in SLI levels in pancreatic, fundic and antral venous plasma, and in IVC plasma; intraduodenal glucose elicited smaller increments. After intragastric fat, a smaller, more gradual increase in the pancreatic and fundic effluents was observed, whereas the rise in antral SLI was minute, and IVC SLI did not rise significantly. Intraduodenal fat elicited a prompt increase in the pancreatic and antral vein SLI levels, and a small but significant increase in fundic and IVC plasma which suggests faster release of enteric factors that influence SLI secretion in the pancreas and antrum. Intragastric casein hydrolysate elicited a prompt increase in SLI in both the pancreatic and fundic veins, the latter being marked, but the antral SLI response was small; IVC SLI rose significantly within 15 min. Intragastric HCl provoked a prompt and marked rise in pancreaticoduodenal and antral vein SLI but no increase in fundic vein SLI; IVC SLI levels rose significantly within 20 min. Intraduodenal HCl elicited an even more prompt and marked pancreatic SLI response, and SLI rose significantly in both the fundic and antral venous effluents; IVC SLI also rose more promptly. In dogs with a gastric fistula that prevented intraduodenal entry of HCl, intragastric HCl elicited only a very small and transient rise in pancreaticoduodenal vein SLI, markedly stimulated the antral SLI response, but completely suppressed fundic venous SLI levels. The results indicate that all three nutrients stimulate SLI release from the pancreas and stomach. The greater SLI response to intragastric, as opposed to intraduodenal, glucose suggests that unidentified local factors are of importance. The responses to the intraduodenal instillation of HCl and fat suggest a role of enteric hormones in the release of SLI from the pancreas and fundus and antrum of the stomach. Additionally, there is evidence of direct effects of HCl upon gastric SLI release.