Elevated neuropeptide levels decrease during liver transplant.
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Analysis of Variance↗
Biomedical subjects
W Stapelfeldt
Publications and source records attributed to W Stapelfeldt.
Effect of naloxone on vagally-induced gastric acid secretion in rats.
Previous studies in man and dogs have demonstrated that endogenous opioids participate in the stimulation of cephalic phase gastric acid secretion during indirect activation of the vagus. Since the effect of naloxone during direct vagal activation is unknown gastric acid secretion was assessed during electrical stimulation of the distal cut ends of both vagal nerves. In overnight fasted anesthetized rats the distal ends of the bisectioned cervical vagi were stimulated with 10V, 5Hz, 5 msec for 15 min. Vagal stimulation elicited an increase of gastric acid secretion by 5.6 mumol/min. Naloxone (1 mumol/kg.h) augmented gastric acid secretion significantly. Since this effect of naloxone was in contrast to previous data possible mechanisms of action of naloxone were examined that might help to explain this apparently inhibitory action of endogenous opioids on vagally-induced gastric acid secretion. The additional infusion of atropine or hexamethonium abolished the stimulatory effect of naloxone on vagally-induced acid secretion completely indicating that the action of naloxone depends on cholinergic background activity. Combined blockade of alpha- and beta-adrenergic receptors with phetolamine and propanolol reduced vagally-induced acid secretion in controls and during naloxone to a similar degree. Both adrenergic blocking agents also reduced the residual acid secretion observed during atropine or atropine + naloxone infusion. Measurements of plasma gastrin levels suggested that the naloxone-induced changes of acid secretion were not due to alterations of gastrin secretion. In summary these data demonstrate that vagally-induced acid secretion in anesthetized rats is largely due to cholinergic mechanisms with a small but separate contribution of adrenergic mechanisms. Endogenous opioids are activated during peripheral vagal stimulation attenuating vagally-induced acid secretion by modulation of cholinergic but not adrenergic mechanisms.
Animals↗
Effect of atrial peptide on gastric acid secretion in rats.
The effect of synthetic rat atriopeptin (AP) II was examined on basal, vagally and carbachol-induced gastric acid secretion in anesthetized rats. AP II infusion, at stepwise increasing doses of 2, 20 and 100 ng/kg/min, had no effect on basal acid secretion. At doses of 2 and 20 ng/kg/min, AP II augmented vagally induced acid secretion significantly. The secretory response to vagal stimulation + AP II 20 ng/kg/min was completely abolished by atropine. In contrast a higher dose of AP II (50 ng/kg/h) reduced vagally induced acid secretion significantly. This dose of AP II also reduced acid secretion during direct cholinergic stimulation by carbachol, while the lower dose of 20 ng/kg/min had no effect on carbachol-induced acid secretion. The present data demonstrate for the first time an effect of atrial peptide on gastric acid secretion. At lower doses AP II augments the vagal influence on parietal cell function perhaps by augmenting vagally induced acetylcholine release. At higher doses AP II exerts an inhibitory effect on parietal cell function during vagally and carbachol-induced acid secretion, suggesting different and as yet unknown mechanisms of action. These results raise the possibility that the heart can exert a hormonally mediated influence on the regulation of gastric acid secretion.
Animals↗
Effect of continuous and oscillatory portal vein insulin infusion upon glucose-induced insulin release in rats.
The present study was designed to determine the effect of low dose continuous and oscillatory intraportal insulin infusions upon subsequent glucose-induced insulin release. In overnight-fasted and anesthetized rats with indwelling catheters in the jugular vein, carotid artery, and mesenteric vein insulin was infused intraportally for 3 h via the mesenteric vein catheter at a continuous rate of 45 microU/kg X min, or the same amount of insulin was administered at alternating high (72 microU/kg X min) and low infusion rates (18 microU/kg X min), respectively, in 2-, 4-, 8-, and 16-min cycles (oscillatory infusions). Another group received a continuous infusion of saline. Glucose (0.4 g/kg) was given i.v. 30 min after the end of the insulin or saline infusion. During the 3-h infusion of insulin or saline the peripheral glucose level remained unchanged in all groups. In response to the i.v. glucose load peripheral arterial plasma insulin levels were significantly elevated after preceding oscillatory infusions compared to the continuous insulin infusion. As compared to the group receiving saline the glucose-induced insulin response after continuous insulin infusion was significantly reduced. The plasma glucose responses were not different except for inexplicably elevated glucose levels in the 4-min cycle group. No difference was observed for plasma glucagon levels in all groups. The present data demonstrate an augmented responsiveness of the beta-cell to glucose after a preceding oscillatory infusion of insulin and an impaired responsiveness to glucose after continuous insulin infusion. This indicates that an oscillatory insulin release might be of importance for an adequate regulation of beta-cell function.
Animals↗
Effect of histamine H2-receptor stimulation on postprandial pancreatic and gastric endocrine function in dogs.
The effect of histamine H2-receptor stimulation via the infusion of impromidine was assessed with regard to postprandial plasma insulin, pancreatic polypeptide (PP), somatostatin, and gastrin levels. The effect of impromidine was assessed in the postprandial state during a liver extract/sucrose test meal which had a buffer capacity to maintain the intragastric pH at a constant level for the time impromidine was infused. Postprandial plasma insulin and gastrin levels were not changed by impromidine (10 micrograms/kg X h-1). Plasma somatostatin levels rose significantly, whereas the postprandial increase of plasma PP levels was attenuated. The effects on somatostatin and PP were antagonized by the infusion of cimetidine, a specific histamine H2-receptor blocker. In conclusion the present data demonstrate that in the postprandial state activation of H2-receptors stimulates somatostatin and inhibits PP release while insulin and gastrin release are not affected.
Animals↗
Effect of acetylcholine on the release of pancreatic and gastric somatostatin-like immunoreactivity in normal, chemically sympathectomized and indomethacin-treated dogs.
The present study was designed to determine the effects of intravenously infused acetylcholine on the release of pancreatic and gastric somatostatin-like immunoreactivity (SLI), in anesthetized normal, chemically sympathectomized and Indomethacin-treated prostaglandin deficient dogs. In normal dogs acetylcholine infusion (500 micrograms/min) elicited a significant rise in pancreatic vein, inferior vena cava, fundic and antral vein SLI levels. In the sympathectomized animals the rise in pancreatic and antral vein SLI was not different from the controls, while the rise in fundic vein SLI was abolished, and inferior vena cava plasma SLI levels were reduced. During Indomethacin-induced prostaglandin deficiency, basal SLI levels were reduced significantly, and the acetylcholine-induced stimulation was completely abolished from both stomach and pancreas. It is concluded that in anesthetized dogs the intravenous infusion of acetylcholine stimulates pancreatic and gastric SLI release, and this stimulatory effect depends on the presence of prostaglandins and is modulated by adrenergic mechanisms.
Acetylcholine↗
Effect of physiological increments of blood glucose on plasma somatostatin and pancreatic polypeptide levels in dogs.
The present study was designed to determine the effects of physiological increments of plasma glucose levels upon basal and stimulated plasma somatostatin and pancreatic polypeptide levels. In seven conscious dogs the elevation of plasma glucose levels by 30-40 mg/dl did not change basal somatostatin and pancreatic polypeptide levels. During stimulation of these two hormones by acetylcholine and the octapeptide of cholecystokinin intravenous infusion of glucose elicited a significant decrease of somatostatin levels by 30 pg/ml and of pancreatic polypeptide levels by 300 pg/ml. The present data demonstrate that a physiological elevation of plasma glucose levels inhibits stimulated but not basal somatostatin and pancreatic polypeptide levels which may be of importance for nutrient entry and metabolism.
Acetylcholine↗