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PubMed2006

[Effects of acute hypobaric hypoxia on gastric emptying and intestinal propulsion: experiment with rats].

OBJECTIVE: To investigate the impact of acute hypobaric hypoxia on the gastrointestinal motility. METHODS: Eighty Wistar rats were randomly divided into 4 equal groups to be fed with (99)Tc(m)-labeled test food: ground level control group, put in the hypobaric chamber for 30 minutes; 3000 m simulated altitude group, exposed to the environment of simulated altitude of 3000 m for 30 minutes; 5000 m simulated altitude group, exposed to the environment of simulated altitude of 5000 m for 30 minutes; and mosapride + 5000 m simulated altitude group, fed with mosapride 2 mg/kg by perfusing stomach and fed with isotope-labeled test food 30 minutes later, and then exposed to 5000 m simulated altitude for 30 minutes. By the end of experiment the rats were killed, their stomachs were taken out to calculate the gastric emptying rate. Their intestine from pylorus to ileocecum was taken out to measure the intestinal propulsion function by using charcoal particle method. At the beginning and at the end of experiment abdominal arterial blood samples were collected to detect the plasma motilin and nitric oxide (NO) concentrations. RESULTS: The gastric emptying rate of the 5000 m simulated altitude group was 41% +/- 10%, significantly lower than that of the ground level group (62% +/- 12%, P < 0.01), and the charcoal transit rate of the 5000 m simulated altitude group was 37% +/- 8%, significantly lower than that of the ground level group (61% +/- 13%, P < 0.01). The gastric emptying rate and intestine propulsion rate of the 3000 m simulated altitude group were not significantly different from those of the ground level group. The gastric emptying rate of the mosapride + 5000 m simulated altitude group was 55% +/- 12%, significantly higher than that of the 5000 m simulated altitude group (P < 0.05), however, the intestine propulsion rate of the mosapride + 5000 m simulated altitude group was not significantly different from that of the 5000 m simulated altitude group (P > 0.05). The plasma motilin level of the 5000 m simulated altitude group was 88 pg/ml +/- 19 pg/ml, significantly lower than that of the ground level group (123 pg/ml +/- 28 pg/ml, P < 0.01), in contrast, the plasma NO level of the 5000 m simulated altitude group was 106 micromol/L +/- 24 micromol/L, significantly higher than that of the ground level group (80 micromol/L +/- 18 micromol/L, P < 0.01). CONCLUSION: Acute exposure to hypobaric hypoxia at the height of 5000 m inhibits the gastric emptying and intestinal propulsion. Mosapride may alleviate the inhibitory effect of hypobaric hypoxia on gastric emptying. Decrease of plasma motilin and elevation of NO level may be the main mechanism of inhibition of gastrointestinal motility by hypobaric hypoxia.

Animals↗
PubMed2006

[Expression of gastrin, somatostatin, PCNA and Fas-L in the mucosa of gastric antrum of children with chronic gastritis and duodenal ulcer].

OBJECTIVE: Since application of pediatric gastroscopy in the mid-nineteen nineties, there has been a trend that the prevalence rates of pediatric gastritis and duodenal ulcer (DU) are increasing. The diagnosed rate of pediatric gastritis has accounted for 85% - 95% of the total number of children who received gastroscopy, and the rate of DU accounted for 8% - 22%. Such a high rates of the diseases may influence the development of the children severely. However, the etiology and pathogenesis of pediatric chronic gastritis and DU have not been completely elucidated. The disordered gastrointestinal hormones play a crucial role in the pediatric chronic gastritis and DU. This study focused on the expression of gastrin (GAS), somatostatin (SS) in the mucosa of gastric antrum and PCNA and Fas-L in the sinus ventriculi and their possible roles in the pathogenesis of pediatric chronic gastritis and DU. METHOD: The sinus ventriculi mucosal samples of 83 cases were collected via gastroscopic biopsy from the hospital during the recent two years and the cases were divided into five groups: group A, chronic superficial gastritis, Helicobacter pylori (Hp)(+); group B, chronic superficial gastritis, Hp(-); group C, DU, Hp(+); Group D, DU, Hp(-); Group E, normal sinus ventriculi mucosa, Hp(-). Immunohistochemical staining (En Vision) was carried out for GAS, SS, PCNA and Fas-L, and positive cells of each slide were counted (x 400). Statistically significant differences among groups for continuous data were assessed with the software SPSS10.0. RESULTS: The expressions of GAS and SS in the groups A through E had no significant difference. The expression of PCNA in group A was significantly higher than that in group B (P < 0.05), and no significant differences were found among the other groups. There were no significant differences in expressions of Fas-L among the five groups. CONCLUSION: There seems to be an increasing tendency in the expressions of GAS and SS in children with chronic gastritis and duodenal ulcer. Hp infection promotes the multiplication of the sinus ventriculi mucosal epithelium cells in the pediatric chronic gastritis.

Adolescent↗
PubMed1975

Portal and pancreatic vein catheterization with radioimmunologic determination of insulin.

Percutaneous transhepatic catheterization of the portal vein along with the catheterization of the aorta and the vena cava was performed in six patients, one of whom had hypoglycemic attacks due to Whipple's triad. Blood samples from different branches in the different vessel systems were withdrawn for radioimmunologic determination of insulin. By this method, preoperative localization of the insulin producing pancreatic islet cell tumor was su-cessfully performed. Multiple tumors as well as liver metastases were preoperatively excluded. Recatheterization and blood sampling for radioimmunologic determination of insulin was performed postoperatively to verify the radicality of the operation. Insulin concentrations from the hypoglycemic patients were compared with those of the patients without insulinoma and found to be significantly higher. The procedure is proposed as a useful method for localizing all types of gastrointestinal hormone producing primary or secondary tumors in which a method for hormone determination is available. The postoperative investigation is useful as a check of the operation performed and as a follow-up examination for the early diagnosis of recurrence.

Adenoma, Islet Cell↗
PubMed1991

[Neurotensin liberation during the consumption of mineral water from Bad Mergentheimer Karlsquelle].

The contraction of the gallbladder mainly mediated by CCK after oral administration of pharmacological doses of magnesium sulfate is familiar. The same applies to the cholekinetic action of courses of sulfatic mineral water treatment. It was demonstrated in 12 patients in a controlled study that besides other known secretions of gastrointestinal hormones, there is also a significant rise of the plasma level of neurotensin when Bad Mergentheimer Karlsquelle mineral water containing sulfate (3.7 g SO4/l) is drunk on an empty stomach (300 ml, 26 degrees C). This was significantly greater (basal values 6.8 +/- 4.1 pg/ml and a maximum of 15.7 +/- 8.1 pg/ml after 40 min) than in a control group consisting of the same patients who had drunk tapwater. Whereas the involvement of the neuropeptide neurotensin in the regulation of the exocrine functions of the pancreas has been established, its effect in the regulation of gallbladder contraction is probably of rather minor significance compared to CCK.

Adult↗
PubMed1991

Enhanced GFR response to oral versus intravenous arginine administration in normal adults.

Both oral protein ingestion and intravenous amino acid infusions have been shown to increase glomerular filtration rate (GFR) and renal plasma flow (RPF) in normal subjects. Although the mechanism of this effect is not known, the renal responses to these loads have been associated with increases in peripheral glucagon concentrations. Conflicting data exist concerning the role of glucagon in the hyperfiltration response after an oral protein meal or administration of an intravenous amino acid mixture. Using a single amino acid as the stimulus for hyperfiltration, we compared the renal responses in six normal subjects to 30 gm oral arginine-HCl, intravenous arginine-HCl, and intravenous glucagon infused at the rate of 10 ng/kg/min. GFR, RPF, and glucagon concentration, as well as levels of plasma amino acids and selected gastrointestinal hormones, were measured for six 30-minute clearance periods after each load. Significant rises in mean peak GFR were noted after both oral arginine (104 +/- 5 ml/min x 1.73 m2 to 145 +/- 9 ml/min x 1.73 m2, p less than 0.02) and intravenous arginine (118 +/- 10 ml/min x 1.73 m2 to 134 +/- 11 ml/min x 1.73 m2, p = 0.02) administration. Mean peak RPF rose significantly after oral arginine (510 +/- 26 ml/min x 1.73 m2 to 710 +/- 32 ml/min x 1.73 m2, p less than 0.01) but not after intravenous arginine (616 +/- 60 ml/min x 1.73 m2 to 687 +/- 64 ml/min x 1.73 m2, p = 0.18). Intravenous glucagon infusion also increased both mean peak GFR (99 +/- 9 ml/min x 1.73 m2 to 149 +/- 10 ml/min x 1.73 m2, p less than 0.01) and RPF (514 +/- 48 ml/min x 1.73 m2 to 771 +/- 38 ml/min x 1.73 m2, p less than 0.01) significantly. We found the mean peak percent rise in GFR (43% +/- 13%) and RPF (42% +/- 12%) after oral arginine to be notably greater than that after intravenous arginine (14% +/- 5% and 13% +/- 9%, respectively). However, the mean peak percent rise in glucagon concentration after oral arginine was significantly lower than that after intravenous arginine (62% +/- 25% versus 479% +/- 176%, respectively, p = 0.04). Infusion of glucagon increased GFR (54% +/- 13%) and RPF (55% +/- 12%) to a degree similar to that seen after oral arginine, but again with a significantly higher mean peak percent rise in peripheral glucagon concentrations when compared with the rise after oral arginine (798% +/- 348% vs 62% +/- 25%, p less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Oral↗
PubMed1976

Motilin and motilin analogues: mode of action.

Natural porcine motilin (13-methionine-motilin) and its synthetic position 13-substituted analogues, 13-norleucine-motilin and 13-leucine-motilin, are of equal efficacy for gastrointestinal motor activity. Pharmacological in vitro analysis reveals that motilin effects on the gastrointestinal muscle are not mediated via nervous pathways but are brought about by direct action of the polypeptide on the muscle cell. As the contractile response to motilin can be abolished by the Ca++ antagonistic compound verapamil, a role for motilin in the transport of Ca++ to the cytosol of intestinal smooth muscle might be considered. Ca++ fluxes seem to be linked to intracellular cyclic guanosine-3':5'-monophosphate and the antagonistic cyclic adenosine-3':5'-monophosphate. By contrast, in motilin-stimulated gastric pepsin secretion, there is no evidence for a mediating role of cyclic nucleotides. It is more likely that the pepsigogic effect is brought about by augmented gastric mucosal blood flow.

Animals↗
PubMed1991

The effects of calcium and calcium channel blockade on peptide YY and neuropeptide Y release.

The secretory response of many gastrointestinal hormones has been demonstrated to be mediated by way of calcium-dependent pathways. The present study was done to assess the effects of infusions of calcium (15 milligrams per kilogram per hour) and verapamil (5 milligrams per kilogram per hour) on circulatory and ileal intraluminal release of peptide YY and neuropeptide Y. Five dogs weighing 25 kilograms had distal ileal Thiry-Vella segments of 25 centimeters surgically created. After a two week recovery period, each dog was tested after overnight fasting. The dogs were given one hour infusions of either calcium or verapamil after basal measurements. One hour of postinfusion measurements completed the study. Intravenous calcium did not affect circulating peptide YY or neuropeptide Y, but did significantly increase recoverable ileal peptide YY. Verapamil administration significantly increased both circulating peptide YY and neuropeptide Y levels. The results of our data suggest an independent release of intraluminal and intravascular peptide YY as well as modulation of the circulatory release of both peptide YY and neuropeptide Y by cell membrane calcium channel blockade.

Animals↗
PubMed1991

The secretin precursor gene. Structure of the coding region and expression in the brain.

Secretin is a 27-amino acid gastrointestinal hormone that stimulates the secretion of bicarbonate-rich pancreatic fluid. We isolated and analyzed the coding region of the gene for the rat secretin precursor. The entire coding region spans 692 base pairs and is divided into four regions corresponding to the signal peptide and NH2-terminal peptide, the secretin peptide and processing signal sequences, a part of the COOH-terminal peptide, and the remainder of the COOH-terminal peptide, which are interrupted by three short introns (81, 105, and 104 base pairs). The organization is similar to those of the genes for other members of the secretin family, glucagon and VIP/PHI-27 precursors, supporting the assumption that the genes for the secretin family peptide precursors originated from a common ancestral gene. We also demonstrated that the secretin precursor gene is widely expressed in the brain and in the hypophysis. The regional expression pattern of the secretin precursor gene in the brain is quite different from those of the glucagon and VIP/PHI-27 precursor genes. The secretin precursor gene is highly expressed in the medulla oblongata and pons of the brain and the hypophysis, the expression levels of which are comparable to those in the duodenum. The secretin precursor mRNA in the brain and the hypophysis has the same coding sequence as that in the duodenum, indicating that secretin in the brain and the hypophysis is produced from the same secretin precursor protein as that in the duodenum. This is the first evidence to be reported that the secretin precursor gene is definitely expressed in the brain.

Amino Acid Sequence↗
PubMedDate not supplied

The role of prostaglandins in the study of intestinal water and electrolyte transport in man.

The objective of this paper is to assess current knowledge on the pharmacologic and presumed physiologic effects of prostaglandins (PGs) on water and ion transport in the human intestine, from data in the literature and results of authors' studies. PGs, when administered intraluminally or intravenously, induce a profuse net secretion of water and ions into the jejunum or ileum; there is evidence that this effect is unrelated to changes in motility but due to a direct interaction of PGs with mucosal transport processes. Relations of PGs to cholera toxin, gastrointestinal hormones and adenylate cyclase-cyclic AMP system are reviewed. We propose to consider PGs as one of the most convenient model for studying intestinal secretion in vivo in man, in view of the rapid onset, magnitude, reversibility and reproducibility of their striking effect on mucosal transport.

Adenylyl Cyclases↗
PubMedDate not supplied

Effect of somatostatin-14 on gastric emptying and on gastrin and insulin release after ingestion of a mixed solid-liquid meal in man.

The effect of somatostatin-14 on gastric emptying, as well as on serum concentrations of gastrin, insulin, glucose, calcium, and phosphorus after ingestion of a mixed solid-liquid meal was examined in seven healthy men in a double-blind placebo-controlled study. An i.v. bolus injection of 61 nmol somatostatin was followed by 244 nmol infused at a constant rate over 90 minutes. Gastric emptying of a radiolabelled meal was surveyed with the use of a gamma camera. A weak delaying effect of somatostatin on gastric emptying of a solid meal did not prove to be statistically significant. Somatostatin decreased significantly the postprandial gastrin release: the area under the gastrin curve, AUC0-90, 9954 +/- 2287 ng.l-1 min (placebo) vs 5327 +/- 718 ng.l-1 min (somatostatin), p less than 0.05. At the same time suppression of the postprandial insulin release by somatostatin was observed--area under the insulin curve, AUC0-90, 1450 +/- 161 mU.l-1 min (placebo) vs 501 +/- 60 mU.l-1 min (somatostatin), p less than 0.002. The postprandial increase in serum glucose concentration was initially attenuated, and shifted towards the end of somatostatin infusion, when referred to the placebo situation. Somatostatin did not change significantly the serum calcium or phosphorus concentrations. The results obtained indicate that somatostatin's effect on gastric evacuation is less pronounced in contrast to the significant inhibitory influence of somatostatin on release of gastrointestinal hormones.

Adult↗
PubMed1989

[Biliary secretion. Significance of hypercholeresis from the surgical point of view].

In patients carrying a Kehr tube choledochostomy, the surgeon may observe, but rarely, important hypercholeresis, non-bile-acid dependent, in people with severe advanced chronic hepatic diseases or persistent cholestasis. The amount of bile flowing to the outside can reach two liters and more daily. We have seen this in two patients with compensated hepatic disorders and in another suffering from light cholestasis produced by choledocholithiasis. We have also found the same in three other people with liver and the main biliary extrahepatic tract completely normal. This hypercholeresis is continuous and subject to rapid increases relative to the ingestion of food. Such increases are related to gastrointestinal hormones, specially secretin, which is produced when portions of gastric chyme enters the duodenum.

Aged↗