gastrins and Acute-Disease

Helicobacter pylori is highly adapted to its unusual ecological niche in the human stomach. Urease activity permits H. pylori survival at a pH of <4 in vitro and is required for the organism to colonize in animal models. However, urease does not play an important role in the survival of the organism in a pH range between 4 and 7. Other mechanisms of pH homeostasis remain poorly understood, but preliminary studies indicate that novel proteins are produced when H.pylori cells are shifted from pH 7 to 3, and the gene encoding a P-type adenosine triphosphatase that may catalyze NH4+/H+ exchange across the cytoplasmic membrane has been cloned. Mechanisms of pH homeostasis in other enteric bacteria are reviewed and provide insight into additional pathways that may be used by H. pylori. An important adaptation of H. pylori to the gastric environment may be its ability to alter gastric acid secretion. Acute infection is associated with transient hypochlorhydria, whereas chronic infection is associated with hypergastrinemia and decreased somatostatin levels. Thus, the survival of H. pylori in the gastric environment may be attributed to both the development of specialized intrinsic defenses and the organism's ability to induce physiological alterations in the host environment.

Topics: Acute Disease; Chronic Disease; Cytoplasm; Duodenal Ulcer; Enterococcus faecalis; Escherichia coli; Gastric Acid; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Salmonella; Somatostatin; Urease

The action of acute and chronic administration of ethanol on pancreatic exocrine secretion in humans and several animal species is reviewed. If the data concerning the secretory action of ethanol on the pancreas are to the property assessed, several experimental variables have to be considered. Acute intravenous administration of ethanol inhibits basal and hormonally stimulated pancreatic secretion of bicarbonate and protein in nonalcoholic humans and most species of animals tested. Oral or intraduodenal ethanol causes moderate stimulation of pancreatic bicarbonate and enzyme secretion. Since anticholinergic agents and truncal vagotomy diminish the ethanol-induced inhibition of pancreatic secretion in the intact animal, it is possible that the action of ethanol on the pancreas is at least partly mediated by inhibitory cholinergic mechanisms. The action of ethanol on the pancreas may also be mediated by release of gastrointestinal hormones. Intravenous and oral administration of ethanol releases gastrin in dogs but not in humans. Pancreatic polypeptide is unlikely to be the hormonal mediator of the ethanol-induced inhibition of exocrine pancreatic secretion in humans and dogs, since ethanol does not release pancreatic polypeptide. The main secretory changes induced by chronic alcoholism in humans and dogs are increased basal secretion of pancreatic enzymes and decreased basal bicarbonate output, and these secretory changes may favour the occurrence of protein precipitates which are believed to be the first lesion of chronic pancreatitis in man. A decrease in the concentration of "pancreatic stone protein" in pancreatic juice may favour the development of protein precipitates in chronic alcoholic patients.

Topics: Acute Disease; Alcoholism; Animals; Calcium-Binding Proteins; Cholecystokinin; Chronic Disease; Dogs; Duodenum; Ethanol; Food; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Lithostathine; Nerve Tissue Proteins; Pancreas; Pancreatic Juice; Pancreatic Polypeptide; Pancreatitis; Secretin; Sphincter of Oddi; Stomach

Topics: Acute Disease; Amylases; Antacids; Anti-Ulcer Agents; Calcitonin; Depression, Chemical; Enzyme Inhibitors; Gastric Acid; Gastrins; Hormones; Humans; Pancreas; Pancreatitis; Zollinger-Ellison Syndrome

Cimetidine is a specific competitive histamine H2-receptor antagonist which effectively inhibits gastric acid secretion and is advocated for the treatment of chronic peptic ulceration, haemorrhage from erosive gastritis, and the control of gastric hypersecretion and peptic ulceration in the Zollinger-Ellison syndrome. Placebo-controlled trials in outpatients have demonstrated its efficacy in promoting the healing of endoscopically diagnosed duodenal ulceration, during a period of 4 to 6 weeks, but its role in the treatment of gastric ulcer is less clear. Preliminary evidence suggests that maintenance therapy with cimetidine reduces the rate of recurrence of duodenal ulcer, but further studies are required to clarify its role in this situation and in the treatment of oesophagitis and acute gastrointestinal haemorrhage. Cimetidine controls the peptic ulceration of Zollinger-Ellison syndrome in most patients when given continuously for up to 2 years. Side-effects have generally been trivial and have very seldom necessitated withdrawal of therapy except in the rare occurrence of gynaecomastia. The haematological abnormalities particularly agranulocytosis, which lead to the withdrawal from clinical use of metiamide, have not been reported with cimetidine, except for 1 case of transient neutropenia. The safety of long-term cimetidine administration has yet to be determined.

Topics: Acute Disease; Animals; Cimetidine; Duodenal Ulcer; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Guanidines; Humans; Intrinsic Factor; Recurrence; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Acute Disease; Alcoholism; Animals; Autoradiography; Bicarbonates; Chronic Disease; Dogs; Enzyme Inhibitors; Ethanol; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Humans; Pancreas; Pancreatic Juice; Pancreatitis; Proteins; Rabbits; Rats; Secretory Rate; Sphincter of Oddi

Topics: Acute Disease; Adenoma, Islet Cell; Cholecystokinin; Chronic Disease; Gastrins; Humans; Methods; Pancreas; Pancreas Transplantation; Pancreatic Diseases; Pancreatic Neoplasms; Pancreatitis; Radiography; Secretin; Transplantation, Homologous; Zollinger-Ellison Syndrome

Pantoprazole is a new substituted benzimidazole which is a potent inhibitor of gastric acid secretion by its action upon H+,K(+)-ATPase.. The proton pump inhibitors pantoprazole and omeprazole were compared in a randomized, double-blind study in 219 patients with benign gastric ulcers. Patients received either pantoprazole 40 mg (n = 146) or omeprazole 20 mg (n = 73), once daily before breakfast for 4 weeks. Treatment was extended for a further 4 weeks if the ulcer had not healed.. After 4 weeks, complete ulcer healing was seen in 88% of protocol-correct patients given pantoprazole and in 77% given omeprazole (between-group difference P < 0.05). At 8 weeks, the corresponding values were 97% and 96% (not significant). In the comparative intention-to-treat analysis there were no statistical differences between the treatment groups. Among the patients who had ulcer pain prior to treatment, 79% of the pantoprazole group and 68% of the omeprazole group were pain-free after 2 weeks, and after 4 weeks 88% and 81%, respectively (not significant). Pronounced improvement in the other gastrointestinal symptoms was seen in both groups. Only 10% of patients in each group reported adverse events. There were moderate increases in fasting serum gastrin levels with both treatments at 4 and 8 weeks.. Pantoprazole, 40 mg once daily in the morning, is a highly effective, well tolerated treatment for acute, benign gastric ulcer. Pantoprazole and omeprazole were equally safe in the therapy of gastric ulcer.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Acute Disease; Administration, Oral; Adult; Aged; Aged, 80 and over; Benzimidazoles; Double-Blind Method; Female; Gastrins; Humans; Male; Middle Aged; Omeprazole; Pain; Pantoprazole; Proton Pump Inhibitors; Stomach Ulcer; Sulfoxides

To study in a double-blind controlled manner the effects of lansoprazole 15 mg or 30 mg daily compared with ranitidine 300 mg once daily and placebo in the relieving of symptoms and healing of acute duodenal ulceration.. Two hundred eighty patients with duodenal ulcer entered in to the study from 30 centers. They were randomized in a double-blind manner into four groups with 80 patients entered into each active treatment group and 40 patients into the placebo group. Endoscopy was performed at 2- and 4-wk intervals to assess healing. Symptom relief was recorded, serum gastrin levels were measured, and gastric mucosal biopsies were obtained to evaluate for the presence of acute and chronic inflammation, the presence of neoplasia, and the extent of gastric endocrine growth at the time of endoscopy.. After 4 wk of treatment using per protocol analysis, 19 of 40 (47.5%) patients receiving placebo had healed compared with 55 of 78 (70.5%) receiving ranitidine (p < 0.05 vs. placebo), 61 of 76 (80.3%) receiving lansoprazole 30 mg (p < 0.05 vs. placebo), and 72 of 78 (92.3%) receiving lansoprazole 15 mg (p < 0.05 vs. placebo and ranitidine). In patients with evaluable data, lansoprazole 30 mg and ranitidine produced greater relief of night-time symptoms and lansoprazole 15 mg produced greater relief of both day- and night-time symptoms than did placebo after 4 wk of treatment. Ranitidine increased fasting serum gastrin levels (22%; p < 0.05 vs. placebo), whereas both lansoprazole regimens produced more marked rises in serum gastrin (54% and 60%; p < 0.05 vs. placebo and ranitidine). Lansoprazole 15 mg and 30 mg also increased the density of antral G-cells (105.8% and 128.80%; p < 0.05 vs. baseline) and greater curvature Grimelius-positive cells (20.33% and 28.8%; p < 0.05 vs. baseline); there were no increases in the density of antral EC- or D-cells, and there was no alteration of gastric endocrine growth as judged by the Solcia classification. Both ranitidine and lansoprazole were associated with decreased antral Helicobacter pylori density accompanied, in the lansoprazole groups, by decreased antral inflammation scores. All antisecretory regimens were associated with increased inflammatory scores in the greater curvature.. In acute duodenal ulceration, treatment with lansoprazole 15 and 30 mg produced 4-wk healing rates and symptom relief superior to those produced by placebo and the 15-mg dose similar to those produced by placebo. The 15-mg dose of lansoprazole was also superior to ranitidine in healing duodenal ulcer after 4 wk of therapy.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Acute Disease; Adult; Anti-Ulcer Agents; Double-Blind Method; Drug Administration Schedule; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Helicobacter pylori; Humans; Lansoprazole; Male; Omeprazole; Ranitidine

During organic stress, severe dysfunctions of fundamental biological phenomena, such as modification of vagal tone, have been described. These dysfunctions could induce changes in the rhythm of acid secretion and/or its hormonal control. We therefore analyzed the effects of acute respiratory failure on the 24 h variations in intragastric pH, serum gastrin, and pancreatic polypeptide levels, taken as a marker of vagal tone. Body temperature and plasma cortisol circadian rhythms were used as marker rhythms. Twelve patients with chronic obstructive pulmonary disease complicated with acute respiratory failure were studied before and during continuous enteral nutrition; half of the patients received ranitidine, a H2 blocker. During the 3 days of the study, intragastric pH was below 2.5 for only one third of the time. No difference was observed between the placebo and the ranitidine groups. Plasma pancreatic polypeptide was within normal ranges despite increased cortisol levels. Gastrin levels reflected changes in intragastric pH over the 24 h time frame and were noted to increase during ranitidine and enteral nutrition. Despite the loss of cortisol and body temperature circadian rhythmicity all throughout the study, circadian rhythms were maintained or restored during the different therapeutic regimens for intragastric pH, serum gastrin, and pancreatic polypeptide levels. Moreover, an ultradian rhythm for gastrin before any treatment, a circadian rhythm for intragastric pH on enteral nutrition, a circadian rhythm for intragastric pH, plasma gastrin and plasma pancreatic polypeptide on ranitidine regimen were observed. Thus during acute respiratory failure, certain physiological circadian rhythms persisted despite the disappearance of "marker" rhythms. Furthermore, these rhythms for digestive secretions could be pharmacologically restored.

Topics: Acute Disease; Aged; Body Temperature; Circadian Rhythm; Double-Blind Method; Enteral Nutrition; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Humans; Hydrocortisone; Male; Middle Aged; Pancreatic Polypeptide; Random Allocation; Ranitidine; Respiratory Insufficiency; Stress, Physiological

The ability of H2 receptor antagonists and continuous enteral alimentation to maintain high intragastric pH in patients with chronic obstructive pulmonary disease (COPD) requiring mechanical ventilation was evaluated by continuously monitoring intragastric pH prior to and following sequential addition of ranitidine or continuous enteral alimentation (or both) to their therapeutic regimen. Prior to therapy, intragastric pH was less than 4.0 for 75 +/- 10 percent of the time, but never less than 1.0. Nevertheless, this moderate gastric acidity was associated with evidence of mucosal injury. Ranitidine failed to continuously maintain a high intragastric pH (pH less than 4.0 for 35 +/- 11 percent of the time; p greater than 0.2 compared to patients treated with placebo). Following administration of continuous enteral alimentation, intragastric pH fell, and ranitidine therapy only partially blocked this increase in gastric acidity induced by continuous enteral alimentation. We conclude that without treatment, patients with COPD who have acute respiratory failure may develop gastric mucosal injury despite the presence of only moderate intragastric acidity; however, ranitidine and continuous enteral alimentation are not effective in maintaining a high intragastric pH.

Topics: Acute Disease; Adult; Aged; Combined Modality Therapy; Enteral Nutrition; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Humans; Hydrogen-Ion Concentration; Lung Diseases, Obstructive; Male; Middle Aged; Ranitidine; Respiration, Artificial; Respiratory Insufficiency; Time Factors

To compare effects of different point combinations of Zusanli (ST 36) for improving acute gastric mucosa injury and study on the mechanism.. One hundred rats were randomly divided into 10 groups, Zusanli (ST 36) group (group A); Zusanli and Neiguan (PC 6) group (group B); Zusanli and Zhongwan (CV 12) group (group C); Zusanli and Gongsun (SP 4) group (group D); Zusanli, Neiguan and Zhongwan group (group E); Zusanli, Neiguan and Gongsun group (group F); Zusanli, Zhongwan and Gongsun group (group G); Zusanli and Neiguan, Zhongwan, Gongsun group (group H); model group (group I); blank control group (group J), 10 rats in each group. Gastric mucosa injury model was made by intragastric infusion of dehydrated alcohol (0. 6 mL/100 g). The gastric mucosa injury index (UI), epidermal growth factor (EGF), nitric oxide (NO) and gastrin (GAS) contents were detected.. Contents of EGF and NO were significantly increased and GAS content decreased in all of the EA groups as compared with those in the model group (P<0. 01 or P<0. 05), with no significant differences among group A, B and D, and significant differences as group A compared with group C, F and group H compared with other EA groups.. Different point combinations of Zusanli (ST 36) can improve acute gastric mucosa injury, with the strongest effect in the Zusanli and Neiguan, Zhongwan, Gongsun group.

Topics: Acupuncture Points; Acute Disease; Animals; Epidermal Growth Factor; Ethanol; Female; Gastric Mucosa; Gastrins; Male; Nitric Oxide; Rats; Rats, Sprague-Dawley

Ghrelin, identified in the gastric mucosa, has been involved in the control of food intake and growth hormone (GH) release, but whether this hormone influences the gastric secretion and gastric mucosal integrity has been little elucidated. We compared the effects of intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) administration of ghrelin on gastric secretion and gastric lesions induced in rats by 75% ethanol or 3.5 h of water immersion and restraint stress (WRS) with or without suppression of nitric oxide (NO)-synthase or functional ablation of afferent sensory nerves by capsaicin. The number and the area of gastric lesions was measured by planimetry, the GBF was assessed by the H2-gas clearance method and blood was withdrawn for the determination of the plasma ghrelin and gastrin levels. In addition, the gastric mucosal expression of mRNA for CGRP, the most potent neuropeptide released from the sensory afferent nerves, was analyzed in rats exposed to WRS with or without ghrelin pre-treatment. Ghrelin (5-80 microg/kg i.p. or 0.6-5 microg/kg i.c.v.) increased gastric acid secretion and attenuated gastric lesions induced by ethanol and WRS. This protective effect was accompanied by a significant rise in the gastric mucosal blood flow (GBF), luminal NO concentration and plasma ghrelin and gastrin levels. Ghrelin-induced protection was abolished by vagotomy and significantly attenuated by L-NNA and deactivation of afferent nerves with neurotoxic dose of capsaicin. The signal for CGRP mRNA was significantly increased in gastric mucosa exposed to WRS as compared to that in the intact gastric mucosa and this was further enhanced in animals treated with ghrelin. We conclude that central and peripheral ghrelin exerts a potent protective action on the stomach of rats exposed to ethanol or WRS, and these effects depend upon vagal activity and hyperemia mediated by the NOS-NO system and CGRP released from sensory afferent nerves.

Topics: Acute Disease; Animals; Calcitonin Gene-Related Peptide; Capsaicin; Dose-Response Relationship, Drug; Enzyme Inhibitors; Ethanol; Gastric Acid; Gastric Mucosa; Gastrins; Gastrointestinal Diseases; Gene Expression; Ghrelin; Immersion; Injections, Intraperitoneal; Injections, Intraventricular; Male; Nitric Oxide; Nitric Oxide Synthase; Nitroarginine; Peptide Hormones; Rats; Rats, Wistar; RNA, Messenger; Stress, Physiological; Vagotomy; Water

To evaluate the effect of early intrajejunal nutrition (EIN) on the natural course, entero-hormone secretion and its efficacy on dogs with acute pancreatitis.. An acute pancreatitis model was induced by injecting 1 ml/kg of combined solution (2.5% sodium taurocholate and 8,000-10,000 BAEE units trypsin/ml) into the pancreas via pancreatic duct. Fifteen dogs were divided into parenteral nutrition (PN) group and EIN group. Two groups were isonitrogenous and isocaloric. EIN was used at postoperative 24 h. Serum glucose, calcium, amylase and lysosomal enzymes were determined before and 1, 4, 7 d after acute pancreatitis was induced. All the dogs were injected 50 uCi 125I-BSA 4 h before sacrificed on the 7th day. The 125I -BSA index of the pancreas/muscle, pancreas/blood, and pancreas pathology score (PPS) were determined. The peripheral plasma cholecystokinin (CCK), secretin (SEC) and gastrin were measured by ELISA and RIA, and was quantitative analysis of pancreatic juice and amylase, pancreatolipase and HCO3-, Cl-, Na+ and K+ performed by an autochemical analyzer at 30, 60, 120 and 180 min after beginning PN or EIN on the first day.. There was no difference between two groups in the contents of serum calcium, amylase and lysosomal enzymes, 125I-BSA index of pancreas/muscle and pancreas/blood and PPS. The contents of CCK and gastrin in EIN were higher than those in PN group at 60 and 120 min (P<0.05). The content of SEC post-infusion of nutrition solution was higher than that of pre-infusion of nutrition solution in both groups, and only at 60 min SEC in EIN group was higher than that in PN group. The content of gastrin in EIN was higher than that in PN group at 120 and 180 min (P<0.05). The changes of pancreatic juice, amylase, pancreatolipase and HCO3-, Cl-, Na+ and K+ between two groups did not reach significantly statistical difference (P>0.05).. EIN does not stimulate entero-hormone and pancreatic juice secretion, and enzyme-protein synthesis and release. EIN has no effect on the natural course of acute pancreatitis.

Topics: Acute Disease; Amylases; Animals; Blood Glucose; Calcium; Cholecystokinin; Dogs; Gastrins; Iodine Radioisotopes; Jejunum; Lysosomes; Pancreatic Juice; Pancreatitis; Parenteral Nutrition; Secretin; Serum Albumin, Bovine

We describe a patient with multiple endocrine neoplasia type 1 characterized by the simultaneous occurrence of parathyroid cancer, parathyroid adenomas, and pancreatic gastrinoma, who presented with an episode of acute hypercalcemia. The rapid parathyroid hormone assay provided a basis for the diagnosis of parathyroid hyperfunction. Mediastinal metastasis of the parathyroid carcinoma was found at autopsy. However, the staining of pancreatic and gastric tissue for parathyroid hormone-related protein does not make it possible to exclude completely the contribution of this peptide in mediating the hypercalcemia. To our knowledge, this is the first reported case of parathyroid carcinoma as part of the multiple endocrine neoplasia type 1 syndrome.

Topics: Acute Disease; Adenoma; Adult; Carcinoma; Fatal Outcome; Gastrinoma; Gastrins; Humans; Hypercalcemia; Hyperparathyroidism; Male; Multiple Endocrine Neoplasia Type 1; Pancreatic Neoplasms; Parathyroid Hormone; Parathyroid Neoplasms

Ischemia followed by reperfusion is known to produce gastric lesions due to oxidative stress, but the role of gastric H(+) secretion in the formation of this mucosal injury remains unknown. We studied alterations in gastric acid secretion and gastric histamine content, as well as the expression of histidine-decarboxylase and interleukin-1beta during the mucosal recovery from ischemia-reperfusion erosions. Gastric secretion was studied in rats (series A) with gastric fistula before, during and after the ischemia induced by clamping of celiac artery for 0.5 h followed by reperfusion in animals pretreated with vehicle (saline), omeprazole, a proton pump inhibitor, or ranitidine, a histamine (H(2)) receptor antagonist. In series B, the animals were submitted to 0.5 h of ischemia followed by 1 h of reperfusion and then anesthetized at 0, 3, 12 and 24 h or 3, 5, 10 or 15 days after the end of ischemia-reperfusion to determine gastric blood flow by H(2)-gas clearance technique, area of gastric lesions, plasma gastrin and interleukin-1beta levels, histamine content by radioimmunoassay (RIA) and expression of histidine-decarboxylase and interleukin-1beta mRNA by reverse transcription polymerase chain reaction. Clamping of celiac artery caused cessation of gastric blood flow and almost complete suppression of basal gastric acid secretion (series A) that returned gradually to the control value at day 3 after ischemia-reperfusion, accompanied by the rise in plasma gastrin levels, pronounced expression of histidine-decarboxylase mRNA and increased mucosal histamine content. Ischemia, followed by 1 h of reperfusion, produced gastric erosions (series B) that reached maximum at 12 h, but then declined at 24 h. These erosions progressed at day 3 into deeper ulcers whose area declined progressively within the next 5-15 days. The gastric blood ceased to flow (series B) during 30 min of clamping and was reduced throughout the period of healing of acute erosions, being accompanied by a gradual rise in mucosal interleukin-1beta mRNA content and in plasma interleukin-1beta levels. Treatment with omeprazole or ranitidine, which completely suppressed gastric acid secretion and significantly raised plasma gastrin level, greatly reduced the formation of erosive lesions preventing the progression of these lesions to chronic gastric ulcers, and this was accompanied by the rise in gastric blood flow and plasma gastrin levels and the significant attenuation of plasma interleukin-1beta

Topics: Acute Disease; Animals; Anti-Ulcer Agents; Blood Flow Velocity; Disease Progression; Gastric Acid; Gastric Mucosa; Gastrins; Gene Expression Regulation; Histamine; Histidine Decarboxylase; Interleukin-1; Male; Omeprazole; Polymerase Chain Reaction; Ranitidine; Rats; Rats, Wistar; Reperfusion Injury; RNA, Messenger; Stomach; Stomach Diseases; Stomach Ulcer; Time Factors

Hepatic porphyrias are characterized by neurological symptoms manifested by abdominal pain, neuropathies and mental aberrations. Porphyrins are ubiquitous and essential biochemical constituents of living beings acting as mediators of oxidation reaction in the metabolism of the steroid, drugs, environmental chemicals or as a mean of exchanging gases, such as oxygen and carbon dioxide between the environment and the tissue of the body using endogenous polypeptide properties. The different porphyrins arising from the arrangement of normal heme synthesis are characterized by an accumulation and excretion of specific intermediate porphyrins and/or of precursors exerting toxic effect, initiating cascades of generations of polypeptides, neurotransmitters and gut-brain axis peptide responsible for the symptoms of clinical status. We studied polypeptide levels in 27 patients (19 females, 8 males) presenting acute attack of hepatic porphyria: 2 with ALA dehydratase-deficient porphyria; 9 with acute intermittent porphyria; 12 with porphyria cutanea tarda and 4 with variegate porphyria. During acute attacks of porphyria, polypeptides were found to be constantly increased: vasoactive intestinal polypeptide (VIP); neurotensin (NT); substance P; pancreatic polypeptide; gastrin-releasing peptide; gastrin and motilin. Administration of the somatostatin (antagonizing polypeptide), which was undetectable or low before treatment, apparently alleviated the acute symptomatology. Elevated levels of polypeptides, at least partly, contribute to appearance of acute symptoms in porphyria patients.

Topics: Acute Disease; Adolescent; Adult; Female; Gastrin-Releasing Peptide; Gastrins; Humans; Male; Middle Aged; Motilin; Neurotensin; Pancreatic Polypeptide; Peptides; Plasmapheresis; Porphyrias, Hepatic; Porphyrins; Somatostatin; Substance P; Vasoactive Intestinal Peptide

Melatonin, a pineal hormone, synthesized from L-tryptophan, is known to exist in the gut and to scavenge oxygen free radicals but its role in gastroprotection against acute lesions induced by various strong irritants has been little studied. In this study, we determined the effects of melatonin and L-tryptophan on gastric secretion and the formation of acute gastric lesions induced by absolute ethanol, acidified aspirin (ASA), stress, and ischemia-reperfusion (I/R). Area of gastric lesions was determined by planimetry, gastric blood flow (GBF) was measured using a H2-gas clearance technique, and blood was withdrawn for the measurement of free radicals, plasma gastrin, and melatonin concentration by specific radioimmunoassay. Intragastric (i.g.) administration of melatonin (2.5-10 mg/kg) or L-tryptophan (25-200 mg/kg) failed to affect gastric lesions by ethanol and ASA but dose-dependently reduced the lesions provoked by stress and I/R; this protective effect was accompanied by a significant rise in plasma melatonin level, GBF, and DNA synthesis and by a marked fall in blood free radicals. L-tryptophan, which significantly elevated the plasma melatonin by about 3-5-fold, also reduced the stress and I/R-induced lesions and blood levels of free radicals, while increasing the GBF, DNA synthesis, and plasma gastrin levels. Inhibition of mucosal generation of PGE2 by indomethacin abolished the protection and the rise of GBF afforded by melatonin and L-tryptophan, whereas pretreatment with N(G)-nitro-L-arginine (L-NNA), to suppress nitric oxide (NO) synthase, was without any effect. We conclude that melatonin applied exogenously in pharmacological doses and that released by the administration of its precursor, L-tryptophan, protect gastric mucosa from the damage induced by stress and I/R possibly by a mechanism involving the scavenging of free radicals and gastric hyperemia probably mediated by endogenous prostaglandin but not NO.

Topics: Acute Disease; Animals; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; DNA; Dose-Response Relationship, Drug; Ethanol; Female; Free Radical Scavengers; Gastric Mucosa; Gastrins; Male; Melatonin; Radioimmunoassay; Rats; Rats, Wistar; Reperfusion Injury; Solvents; Stomach; Stomach Ulcer; Stress, Physiological; Tryptophan

Topics: Acute Disease; Adolescent; Adult; Duodenal Ulcer; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer Hemorrhage; Peptic Ulcer Perforation; Recurrence; Reference Values

Abnormal gastric motility has been suggested as a possible causative factor for acute gastric dilatation observed in nonhuman primates. To evaluate gastric motility in a colony, fasting serum gastrin immunoreactivity and gastric emptying times were assessed in rhesus monkeys that had survived single episodes of acute gastric dilatation. These were paired with age- and weight-matched control monkeys from the same colony. Neither gastric emptying times nor gastrin assays were significantly different between the acute gastric dilatation and control groups.

Topics: Acute Disease; Animals; Biomarkers; Gastric Dilatation; Gastric Emptying; Gastrins; Gastrointestinal Motility; Macaca mulatta; Primate Diseases; Reference Values

The objective was to measure gastrin (G) levels in maternal and neonatal sera as well as in amniotic fluid in patients with fetal distress and a control group. Twenty-five patients with term pregnancies were assigned to the following two groups: fifteen with acute fetal distress and ten with previous cesarean section. Maternal and neonatal blood and amniotic fluid samples were taken at the time of delivery. Differences between groups were calculated with non-parametric Mann Whitneys' U test. A significant difference (p < 0.001) between G levels in amniotic fluid of fetal distress and those of the control group was found. In conclusion, serum G levels can be used as another predictor of fetal distress, although further studies must be performed before it can be used as a clinical tool.

Topics: Acute Disease; Amniotic Fluid; Female; Fetal Blood; Fetal Distress; Gastrins; Humans; Pregnancy

The effect of ulcer healing with eradication of Helicobacter pylori (H pylori) on gastric function was investigated in nine patients with duodenal ulcer disease. One month after eradication there were significant reductions in both basal plasma gastrin concentration, from a median (range) of 19 (1-22) to 6 (2-15) pmol/l (p < 0.05), and of basal acid secretion from 8.3 (2.4-24) to 2.6 (1.4-8.1) mM H+/h, (p < 0.01). The peak acid secretion rate was unchanged from 37 (16-59) to 37 (21-59) mM H+/h. After treatment there was no change in the parietal cell sensitivity to stepped infusions of gastrin heptadecapeptide: the median concentration of gastrin required for 50% of maximal acid secretion (EC50) was 41 (14.8-126) before and 33 (23-125) pmol/l after eradication of H pylori. The metabolic clearance rate of gastrin was also unaffected by the eradication of H pylori. Thus eradication of H pylori infection from patients with active duodenal ulcers is accompanied by falls in both basal gastrin release and basal acid secretion without a change in the parietal cell sensitivity to gastrin. Cyclical changes in H pylori infection may cause the variations in basal acid secretion that are seen in duodenal ulcer disease.

Topics: Acute Disease; Adult; Aged; Bismuth; Drug Therapy, Combination; Duodenal Ulcer; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Organometallic Compounds; Parietal Cells, Gastric; Tetracycline

Previous studies demonstrated that epidermal growth factor (EGF) and polyamines (PA) are capable of protecting gastric mucosa against topical irritants. This study was designed to examine whether EGF, PA, and PG affect the healing of acute gastric lesions induced by water immersion and restraint stress. It was found that the healing process of stress lesions in sham-operated rats was significant after 6 hr after stress, and after 24 hr the number of stress lesions was reduced by about 75%. In sham-operated rats, the healing of ulcerations observed at 6, 12, and 24 hr after the stress was accompanied by gradual restoration of DNA synthesis, and both these processes were significantly reduced by administration of DFMO (an inhibitor of ornithine decarboxylase activity) or indomethacin (an inhibitor of cyclooxygenase). In salivectomized rats, the healing was significantly delayed and the DNA was lowered at all time intervals after the stress. Administration of EGF, spermine, aminoguanidine (an inhibitor of degradation of PA), or 16,16-dmPGE2 after stress promoted significantly the healing and DNA synthesis, but pretreatment with DFMO abolished the effect of EGF but not that of spermine. We conclude that EGF, PA, and PG are implicated in healing of stress lesions and that EGF acts, at least in part, by the stimulation of PA formation in the gastric mucosa.

Topics: Acute Disease; Animals; DNA; Drug Therapy, Combination; Epidermal Growth Factor; Gastric Mucosa; Gastrins; Polyamines; Prostaglandins; Rats; Rats, Wistar; Salivary Glands; Stomach; Stomach Ulcer; Stress, Psychological; Time Factors; Wound Healing

Topics: Acute Disease; Age Factors; Bacterial Infections; Calcium; Dysentery; Gastrins; Humans; Infant; Intestinal Diseases; Islets of Langerhans; Pancreas; Trypsin

The serum gastrin content in patients with ulcerous duodenal bleeding was studied in the process of surgical treatment. A significant decrease in the hormone concentration with increase in the volume of acute blood loss was noted.

Topics: Acute Disease; Blood Loss, Surgical; Duodenal Ulcer; Gastrectomy; Gastrins; Humans; Peptic Ulcer Hemorrhage; Postoperative Period

We investigated the time courses of the plasma ethanol, acetaldehyde, gastrin and cholecystokinin (CCK) levels after the ingestion of ethanol (1g/kg, 21.5%, whisky) in healthy male adult volunteers. The ethanol level reached a peak at 15 to 45 minutes after the ingestion and then decreased almost linearly. The acetaldehyde level of the group who became flushed after drinking (the F group) peaked earlier than that of the other group whose faces became only slightly flushed (the N group). The gastrin level increased significantly and remained elevated for about 3 hours. In three of the nine subjects, the CCK level increased 75 minutes after drinking. As a result, the absorption of the ingested ethanol is more rapid than 15 minutes, followed by a quick catabolism of the absorbed ethanol to acetaldehyde, but the catabolic action of acetaldehyde in the F group is later than that in the N group. The plasma gastrin level is certified to increase after the ingestion of ethanol and this is not mediated by acetaldehyde because the intra-venous infusion of acetaldehyde was not increased the plasma gastrin level in dogs. CCK which stimulate the pancreatic enzymes may be considered to have a possibility relating to the development of alcoholic acute pancreatitis but the ingestion of ethanol showed no increase of the plasma CCK level. But we cannot deny the possibility of the individual differences in the hormonal reaction in these experiments.

Topics: Acute Disease; Adult; Alcohol Drinking; Animals; Cholecystokinin; Dogs; Ethanol; Female; Gastrins; Humans; Pancreatitis

To study Ca metabolism in critically ill children, we measured ionized Ca (Ca2+), parathyroid hormone (PTH), calcitonin, 25 hydroxycholecalciferol (25[OH] D3), 1-25 dihydroxycholecalciferol (1-25[OH]2D3, and gastrin levels in critically ill children and in healthy controls. Patients were considered hypocalcemic if Ca2+ was less than 1.1 mmol/L. Six (14%) of 45 patients were hypocalcemic. Five hypocalcemic patients were studied and were found to have higher calcitonin levels than normocalcemic patients and healthy controls and higher PTH levels than healthy controls. 25(OH)D3 and 1-25(OH)2D3 were not significantly different in the three groups of patients. Gastrin levels were low in critically ill patients, whether or not they were hypocalcemic. We conclude that hypocalcemia occurs frequently in critically ill children. It is associated with raised levels of calcitonin and PTH. The mechanism for the increase in calcitonin is unknown.

Topics: Acute Disease; Adolescent; Calcifediol; Calcitonin; Calcitriol; Calcium; Child; Gastrins; Humans; Hypocalcemia; Parathyroid Hormone; Radioimmunoassay

The incretory pancreatic function has been studied in 35 patients with a moderately severe course of acute dysentery. The blood plasma content of insulin, glucagon and gastrin was determined by means of radioimmunoassay with standard kits during the acute course of the disease and prior to discharge of patients. The endocrine pancreatic function was found to be deranged with an increased insulin content during convalescence; the glucagon content was decreased during the period of the disease and the gastrin content was decreased in the acute period.

Topics: Acute Disease; Adult; Dysentery, Bacillary; Gastrins; Glucagon; Humans; Insulin; Reference Values

A series of 31 infants and children with acute duodenal ulcer verified by endoscopy was studied over an eight year period. Eighteen (58%) of them were under 2 years of age. The most common symptom was upper gastrointestinal bleeding (n = 27, 87%). Twenty nine patients (94%) had a preceding illness characterised by diarrhoea, upper respiratory tract infection, or fever, which was not necessarily treated with antipyretic drugs. Initial endoscopy showed that ulcer lesions were solitary in 14 patients and present on the anterior wall (n = 11), posterior wall (n = 2), or both (n = 1). Multiple ulcers were found in 17 patients, and present in the bulb with (n = 6) or without (n = 11) extension into the second part of duodenum. The most conspicuous finding was the irregularly shaped ulcers seen in eight young children with similar clinical and endoscopic features. Sixteen patients were re-endoscoped one to two weeks after the initial examination; the ulcers had entirely disappeared in 13, and there were only small residual ulcers in three. Thirty patients were treated medically and only one (with uncontrollable haemorrhage) required operation. Most patients were symptom free two to six years after the initial diagnosis. Our results suggest that young children may develop acute duodenal ulcers after viral illnesses whether or not they are treated with drugs, mainly antipyretics. This kind of acute duodenal ulcer usually heals quickly irrespective of the morphology, site, and number of ulcers.

Topics: Acute Disease; Adolescent; Child; Child, Preschool; Duodenal Ulcer; Duodenoscopy; Duodenum; Female; Follow-Up Studies; Gastrins; Humans; Infant; Male

To investigate the effects of acute hypercalcemia on exocrine pancreatic secretion, anesthetized cats were given calcium intravenously. Increasing hypercalcemia (3.7-6.3 mmol/L) evoked a dose-dependent increase in enzyme output that was 12 times greater than in normocalcemic controls (p less than 0.001) and was 60% of subsequent maximal stimulation with intravenous cholecystokinin (CCK). The effect of hypercalcemia on enzyme secretion was abolished when CCK was administered 60 min before calcium and at a dose to cause maximal enzyme output. Atropine did not prevent the calcium-induced increase in enzyme secretion. Pancreatic fluid and bicarbonate outputs were not influenced by hypercalcemia during intravenous administration of small amounts of secretin, but were increased by addition of CCK to the secretin infusion. Hypercalcemia did not induce macroscopic or light-microscopic changes in pancreatic morphology. Plasma levels of both CCK and gastrin were increased (p less than 0.01) during hypercalcemia, with and without precalcium administration of CCK; atropine significantly inhibited (p less than 0.05), but did not abolish the calcium-induced releases of both peptides. These data suggest that in the anesthetized cat, acute hypercalcemia induced by intravenous calcium infusion stimulates pancreatic secretion of enzymes, but not fluid and bicarbonate. Acute hypercalcemia also causes release of CCK and, as shown previously, gastrin. The findings suggest that the stimulatory effect of hypercalcemia on pancreatic enzyme secretion is not dependent on intact cholinergic pathways and is probably not exclusively mediated by release of CCK or gastrin.

Topics: Acute Disease; Amylases; Animals; Atropine; Calcium; Cats; Cholecystokinin; Chymotrypsin; Dose-Response Relationship, Drug; Gastrins; Hypercalcemia; Pancreas; Time Factors

Examination of 85 patients with acute intestinal infections (food toxoinfections of medium gravity) of non-established etiology, salmonellosis and acute dysentery) has revealed a significant increase in gastrin concentration in blood plasma both in the acute period and convalescence. The highest increase in blood plasma gastrin concentration was recorded during convalescence, particularly in patients with acute dysentery. Based on the data obtained, the conclusion is made about the involvement of gastrin in the development of gastrointestinal disorders and formation of the adaptation syndrome in acute intestinal infections.

Topics: Acute Disease; Adolescent; Adult; Dysentery, Bacillary; Gastrins; Humans; Intestine, Small; Middle Aged; Salmonella Food Poisoning; Water-Electrolyte Imbalance

Heterogeneity is the most important consideration in the pathophysiology of peptic ulcer disease. Acute ulcers and erosions present clinically with gastrointestinal bleeding or perforation. If they heal there is no predictable recurrence. Factors concerned with mucosal defense are relatively more important than aggressive factors such as acid and pepsin. Local ischemia is the earliest recognizable gross lesion. The gastric mucosa is at least as vulnerable as the duodenal mucosa and probably more so. Most drug-induced ulcers occur in the stomach. Chronic or recurrent true peptic ulcers (penetrating the muscularis mucosae) usually present with abdominal pain. Many duodenal ulcer patients report that the pain occurs when the stomach is empty or is relieved by food, and follows a pattern of relatively long periods of freedom from symptoms between recurrences. Approximately 50% of patients experience a recurrence within a year if anti-ulcer medication is stopped. In most western countries recurrent duodenal ulcer is more common than gastric ulcer. Peptic ulcer disease is also more common in men. Recent evidence indicates genetic and familial factors in duodenal ulcer and increased acid-pepsin secretion in response to a variety of stimuli. However, it is also becoming clear that of all the abnormal functions noted, few are present in all subjects and many are clustered in subgroups. In chronic gastric ulcer of the corpus, defective defense mechanisms, such as duodenogastric reflux and atrophic gastritis, seem to be more important than aggressive factors. Nevertheless, antisecretory medications accelerate the healing of such ulcers. It remains to be seen whether prostaglandins, mucus secretion, or gastric mucosal blood flow are impaired in chronic ulcer disease.

Topics: Acute Disease; Animals; Burns; Chronic Disease; Duodenal Ulcer; Gastric Acid; Gastric Emptying; Gastrins; Humans; Intestinal Mucosa; Peptic Ulcer; Recurrence; Spinal Cord Injuries; Stomach Ulcer; Stress, Physiological

Plasma gastrin immunoreactivity was measured by radioimmunoassay in 45 dogs with acute gastric dilatation-volvulus (GDV). Significant increases (P less than 0.05) were found in dogs with acute GDV and in the fasted state after surgical treatment and recovery. The data suggested that dogs that have had GDV may have preexisting high plasma gastrin immunoreactivity. In dogs with acute GDV, plasma gastrin immunoreactivity was not found to be helpful in formulating prognosis. Circumcostal gastropexy did not affect plasma gastrin immunoreactivity.

Topics: Acute Disease; Aerophagy; Animals; Dog Diseases; Dogs; Gastric Dilatation; Gastrins; Humans; Stomach Volvulus

Topics: Acute Disease; Amylases; Animals; Cholangiopancreatography, Endoscopic Retrograde; Chronic Disease; Gastrins; Pancreas; Pancreatitis; Somatostatin; Swine

Topics: Acute Disease; Adult; Aged; Female; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Insulin; Male; Middle Aged; Pancreatic Polypeptide; Pancreatitis; Vasoactive Intestinal Peptide

The concentration of the NH2-terminal fragment of gastrin-17 in serum was determined by radioimmunochemistry. Two antisera were used, one specific for the COOH-terminus and the other for the NH2-terminus of gastrin-17. The NH2-terminal gastrin-17 immunoreactivity in unfractionated serum correlated well with the amount of fragment found after gel filtration of the same sera (p less than 0.001). In healthy subjects (no. = 100), the NH2- and COOH-terminal gastrin immunoreactivity was 8 +/- 1 and 20 +/- 1 pmol/l (mean +/- SEM), respectively. In patients with acute duodenal ulcer (no. = 30) and acute gastritis (no. = 10) the NH2-terminal immunoreactivity was fourfold increased compared with in healthy subjects (p less than 0.001), whereas the COOH-terminal was identical, the NH2- and COOH-terminal concentrations being 33 +/- 7 and 22 +/- 2 pmol/l in duodenal ulcer and 35 +/- 6 and 21 +/- 1 pmol/l in acute gastritis. Other groups of patients had NH2- and COOH-terminal gastrin concentrations in serum similar to those measured in healthy subjects. The results suggest that gastrin cells process gastrin-17 abnormally during the acute phase of duodenal ulcer and gastritis.

Topics: Acute Disease; Adolescent; Adult; Aged; Amino Acid Sequence; Chromatography, Gel; Duodenal Ulcer; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Peptide Fragments; Radioimmunoassay

Topics: Acute Disease; Animals; Dogs; Fat Emulsions, Intravenous; Female; Gastrins; Male; Pancreatitis; Parenteral Nutrition; Parenteral Nutrition, Total; Trypsin

In order to further investigate hormonal changes and possible metabolic consequences in acute pancreatitis, 10 cases with a mild form of the disease was studied. The influence of tissue injury per se on the hormones in question was assessed from comparison with the hormone levels in the course of myocardial infarction (MI) in 9 cases. Insulin and glucose showed no consistent changes. Glucagon was suppressed on admission, 22 +/- 10 pg . ml-1, compared with the ultimate concentration, 40 +/- 20 pg . ml-1 (p less than 0.05), and with the initial value in MI, 74 +/- 32 pg . ml-1 (p less than 0.01). Serum calcitonin (CT) was strongly elevated initially, 348 +/- 313 pg . ml-1, compared with the ultimate level, 24 +/- 7 pg . ml-1 (p less than 0.001), and with the normal initial level in MI, 43 +/- 44 pg . ml-1 (p less than 0.01). Serum CT elevations were time-related to a slight reduction in corrected serum Ca, which might reflect a biological expression of this substance. In pancreatitis, parathyroid hormone (PTH) remained normal and unchanged throughout the study, whereas patients with MI had an increased level of this hormone on admission, 0.19 +/- 0.08 microgramEq . 1(-1), compared with the ultimate concentration, 0.09 +/- 0.03 microgram/q . 1(-1) (p less than 0.02) and with the initial concentration in pancreatitis, 0.11 +/- 0.06 microgramEq . 1(-1) (p less than 0.05). Supranormal PTH levels were found in more than half of the infarction patients on days 0 and 1.

Topics: Acute Disease; Adult; Aged; Calcitonin; Calcium; Female; Gastrins; Glucagon; Hormones; Humans; Insulin; Male; Middle Aged; Myocardial Infarction; Pancreatitis; Parathyroid Hormone

Topics: Acute Disease; Adolescent; Adult; Aged; Calcium; Diarrhea; Dysentery, Bacillary; Female; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Nucleotides, Cyclic; Shigella flexneri; Shigella sonnei; Syndrome

Topics: Acute Disease; Animals; Gastrins; Gastrointestinal Hormones; Glucagon-Like Peptides; Liver Diseases; Pancreatic Polypeptide; Swine; Vasoactive Intestinal Peptide

Topics: Acute Disease; Animals; Duodenal Ulcer; Gastric Mucosa; Gastrins; Humans; Pylorus

Basal and histalog-stimulated gastric acid secretion and serum gastrin levels before and after a standard protein meal were compared in eight children with active duodenal ulcer (DU), four with active gastric ulcer (GU), and in seven children with recurrent abdominal pain (RAP) of undetermined etiology. There was no discernible difference in the pattern of abdominal pain in DU, GU, and RAP. Basal acid output, peak and maximal acid output, whether expressed as milliequivalents per hour or as milliequivalents per kilogram per hour, were comparable in children with DU, GU, and RAP. In contrast, serum gastrin levels, 1 and 2 hours after standard protein meal, were significantly higher in the DU children than in the GU or RAP group. These studies have suggested that hypersecretion of gastric acid may not be associated with duodenal ulcer or gastric ulcer disease in children, and that increased gastrin secretion and possible reduced acid responsiveness coexist in children with duodenal ulcers.

Topics: Abdomen; Acute Disease; Adolescent; Child; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Humans; Male; Pain; Recurrence; Stomach Ulcer

In 21 female Beagle dogs an experimental pancreatitis was induced by injection of bile into the pancreatic duct system. Beside controls, dogs received 62.5 micrograms/h cyclic somatostatin (SRIF) a continuous i.v. infusion starting with a bolus of 250 micrograms 15 minutes before or 2 hours after bile injection. Following blood parameters were determined: lipase, amylase, blood count, minerals, glucose, insulin, gastrin, secretin and CCK. Two controls died within 24 hours, the others were sacrificed after 48 hours. All pancreata were examined morephologically. The controls developed all clinical signs of acute hemorrhagic pancreatitis, whereas all SRIF-treated dogs were in much better general condition. Lipase and amylase increased in all groups. In the controls insulin, gastrin and secretin remained unchanged and CCK rose slightly. SRIF-treatment diminished insulin, CCK and the test meal-induced increase of secretin. At autopsy the pancreata of the controls were nearly entirely apoplectic. The SRIF-treated dogs showed less damage of the pancreas and no severe hemorrhagic necrosis was noted. The beneficial effect of SRIF cannot only be due to an interaction with intestinal hormones. An additional direct protective effect on the exocrine parenchyma is proposed to exist.

Topics: Acute Disease; Animals; Blood Glucose; Cholecystokinin; Dogs; Fasting; Female; Gastrins; Insulin; Pancreatitis; Secretin; Somatostatin

Thirteen patients with Zollinger-Ellison syndrome (ZES) were treated with cimetidine. This population could be divided into chronic forms, mostly presenting as a common duodenal ulcer, and acute forms resulting in critical problems requiring intensive medical care. Among the 7 patients with chronic ZES, cimetidine treatment was unsuccessful in 2; satisfactory clinical control was obtained in 3 others, but gastrinoma excision was the final treatment; cimetidine treatment has been prolonged for more than 15 months in the last 2 patients. If, in this condition, acute pharmacologic secretory inhibition were constantly obtained, therapeutic efficiency criteria are not sensitive enough to establish certainty in the patient's long-term follow-up. Total gastrectomy is still a valuable alternative if excision of the gastrinoma is not possible. Of the 6 patients with acute ZES, 4 were treated by pirenzepin (0.5 mg/kg intramuscularly 3 times a day) adjunctive to cimetidine infusion (2.4 mg/day), which resulted in increased antisecretory activity. However, total gastrectomy was the final outcome in every patient, with 1 immediate postoperative death. In conclusion, cimetidine in ZES treatment, although capable of inducing ulcer healing, diarrhea disappearance, and dramatic secretory inhibition, is still challenged by surgery, which allows either complete cure of the gastrinoma or definitive suppression of the secretory virulence.

Topics: Acute Disease; Benzodiazepines; Chronic Disease; Cimetidine; Duodenal Neoplasms; Gastrectomy; Gastrins; Guanidines; Humans; Peptic Ulcer; Piperazines; Zollinger-Ellison Syndrome

An ulcer was induced in the anterior wall of the antrum of cats by local injection of acetic acid solution. Carbonized microspheres, 15 +/- 5 microns in diameter, labelled with 141Ce, were used to measure blood flow in different regions and layers of the stomach wall. The radioactivity of a blod reference sample and of tissue samples was determined, and the blood flow was calculated for each tissue sample. The gastric tissue samples were examined microscopically, and the level of gastrin in serum was determined. Two groups of anaesthetized animals were used: in one group of animals blood flow was determined 24 h after ulcer induction and in a group of control animals 24 h after laparotomy. In the ulcer animals the gastric blood flow as increased both in the mucosa and in the muscularis in a zone around the ulcer. Microscopic examination revealed tissue necrosis corresponding to the floor of the ulcer and acute inflammatory changes in the gastric wall around the necrotic area. The serum gastrin concentration tended to increase after ulcer induction.

Topics: Acute Disease; Animals; Cardiac Output; Cats; Female; Gastric Mucosa; Gastrins; Laparotomy; Male; Necrosis; Pyloric Antrum; Regional Blood Flow; Stomach; Stomach Ulcer

Differences in metabolic homeostasis in 12 patients with initial vs. eight patients with repeated attacks of acute pancreatitis have been compared during the acute phase of the disease. As a group, subjects with a previous history of pancreatitis had significantly lower glucagon concentrations (P less than 0.002) for the over all 24-hour study period. Conversely, the serum concentrations of blood sugar, insulin, growth hormone, gastrin, cortisol, nonesterified fatty acids, triglycerides and cholesterol failed to distinguish between the two patient groups. Likewise, immunoreactive plasma parathyroid hormone and calcitonin levels were comparable in both patient populations. Of the measurements considered, it would appear therefore that plasma immunoreactive glucagon is the best indicator of previous pancreatic inflammation. Evaluation of parenchymal integrity during an episode of acute pancreatitis would be of prognostic and therapeutic value in this disease.

Topics: Acute Disease; Adult; Amylases; Blood Glucose; Calcitonin; Calcium; Cholesterol; Fatty Acids, Nonesterified; Female; Gastrins; Glucagon; Growth Hormone; Humans; Hydrocortisone; Insulin; Male; Middle Aged; Pancreatitis; Parathyroid Hormone; Recurrence; Triglycerides

Topics: Acute Disease; Animals; Chronic Disease; Cysteamine; Disease Models, Animal; Duodenal Ulcer; Duodenum; Female; Gastric Juice; Gastrins; Male; Rats

In order to evaluate the effect of acute moderate hypercalcemia on both smooth and skeletal muscle function of the human esophagus, 12 subjects were given intravenous calcium chloride in normal saline. Serum calcium increased from a basal value of 9.6 +/- 0.1 mg per dl (mean +/- 1 SEM) to 11.4 +/- 0.2 mg per dl at 90 min after initiation of calcium infusion (P less than 0.01). Both amplitude and Dp/Dt of esophageal contractions decreased significantly in the skeletal muscle segment; however, amplitude and Dp/Dt increased significantly in the smooth muscle segment. Lower esophageal sphincter pressure remained unchanged. Duration of contractions and peristaltic wave speed were unaltered. Possible explanations for the divergent effect of hypercalcemia on the two types of esophageal muscle are discussed.

Topics: Acute Disease; Adult; Aged; Calcitonin; Calcium; Esophagogastric Junction; Esophagus; Gastrins; Glucagon; Humans; Hypercalcemia; Magnesium; Male; Manometry; Middle Aged; Muscle Contraction; Muscle, Smooth; Muscles; Peristalsis

Topics: Acute Disease; Animals; Dogs; Gastrins; Glucagon; Insulin; Kidney; Liver Diseases

In this study the effect of calcium infusion over 3 h without gastric aspiration on serum gastrin was determined in fifteen normal subjects, ten patients with duodenal ulcer, nine with stomal ulcer, five with total gastrectomy, six with achlorhydria and sixteen with proved or presumed Zollinger-Ellison (ZE) syndrome. Serum gastrin only rose significantly in the patients with ZE-syndrome or achlorhydria. An increase of above or below 50% of basal value seems to be a valuable criterion by which to differentiate between patients with and without ZE-syndrome. Serum gastrin levels in forty-four patients with chronic hypercalcaemia (72+/-24 pg/ml, mean+/-SD) were not significantly different from the levels in 100 normal subjects (66+/-18 pg/ml; P greater than 0.10). However, in one patient with ZE-syndrome and in two patients with achlorhydria serum gastrin values were markedly higher during chronic hypercalcaemia than during normocalcaemia. It is concluded that acute or chronic hypercalcaemia without gastric aspiration does not lead to hypergastrinaemia in the absence of ZE-syndrome or achlorhydria.

Topics: Acute Disease; Calcium; Chronic Disease; Gastrins; Humans; Hypercalcemia; Zollinger-Ellison Syndrome

To better define the pathogenetic relationship between gastric acid secretion, serum gastrin levels and acute gastroduodenal disease in burned patients, fasting serum gastrin levels were correlated with the results of a nonaugmented gastric analysis performed in 31 hemodynamically stable burned patients. Gastroduodenoscopy documented the status of the gastric and duodenal mucosa at the time of acid analysis and serum gastrin collection. Twenty-two patients had acute gastroduodenal disease. Dffuse, superficial, gastroduodenal erosions were present in 17 patients; five additional patients had ulcerative lesions. Nine patients had normal endoscopic examinations. Gastrin levels were not predictive of the incidence, severity or location of disease. Gastric acidity, however, did correlate with disease severity-correlation coefficient, r=+0.41,p less than 0.05-being lowest in normal persons, intermediate in superficial disease and highest in ulceration. There was no correlation between the levels of serum gastrin and gastric acid secretion. The relative hyperacidity in patients with acute gastroduodenal disease suggests that acid may be one of the factors potentiating mucosal injury in these patients and may be particularly important in the evolution of life-threatening ulceration.

Topics: Acute Disease; Adolescent; Adult; Burns; Gastric Juice; Gastrins; Humans; Middle Aged; Peptic Ulcer

Topics: 17-Hydroxycorticosteroids; Acute Disease; Cerebrovascular Disorders; Epinephrine; Gastrins; Gastroscopy; Humans; Norepinephrine; Stomach; Stomach Diseases

Variables of calcium metabolism were measured in 11 patients with clearly documented acute pancreatitis. Total and ionized calcium levels were either low or in the low-normal range as were phosphorus and total magnesium levels. Parathyroid hormone levels were high, and there was a significant inverse correlation with ionized calcium. Gastrin levels were normal, calcitonin values were uniformly below the detection limit of the assay, and pancreatic glucagon levels were elevated. The hypocalcemia of acute pancreatitis was probably not caused by abnormalities of glucagon, calcitonin, or gastrin secretion. Furthermore, parathyroid hormone secretion was apparently not impaired. Hypomagnesemia possibly played a minor role. This study suggests that the hypocalcemia of acute pancreatitis is secondary to extraskeletal calcium sequestration or an as yet unidentified defect of bone metabolism, or both.

Topics: Acute Disease; Calcitonin; Gastrins; Glucagon; Homeostasis; Hypocalcemia; Magnesium; Pancreas; Pancreatitis; Parathyroid Hormone; Phosphorus; Prospective Studies; Triglycerides

In 36 patients with ulcer without Zollinger-Ellison-syndrome (25 patients with recurrent duodenal ulcer, 11 with an ulcus pepticum jejuni after B II-resection of the stomach) and 2 patients suffering from ulcus pepticum jejuni with an ascertained gastrinoma the secretion of acid was compared after stimulation of pentagstrin (6 mug/kg) and calcium (4 mg Ca++/kg/h). The secretion of hydrochloric acid was statistically significantly stimulated in all patients suffering from ulcer by the hypercalcaemia (increase of the serum calcium concentration from 5.0 +/- 0.3 mval/1 to 6.2 +/- 0.8 mval/1). But in patients suffering from ulcer with gastrinoma the stimulatory effect was larger than in such patients without autonomous source of gastrin: the calcium-stimulated secretion of hydrochloric acid was on the average in cases of duodenal ulcer 40% (2 to 68%), in the ulcera peptica jejuni 47% (17 to 75%), in the 4 comparative examinations of the two patients with Zollinger-Ellison-syndrome, however, always more than 100% (106 to 177%) of the pentagastrin-stimulated peak secretion. The comparative test of the pentagastrin and calcium-stimulated secretion of hydrochloric acid could be a help for the proof of autonomous places of the formation of gastrin.

Topics: Acute Disease; Duodenal Ulcer; Gastric Juice; Gastrins; Humans; Hypercalcemia; Jejunum; Peptic Ulcer; Recurrence; Zollinger-Ellison Syndrome

In 29 rabbits the action of PGF2 alpha and PGE2 was compared with prostigmine in a mechanical ileus model. PGE2 produces no therapeutical effect. PGF2 alpha delivered a significant increase of intraluminal intestinal pressure and of the amplitudes of peristalsis, lasting for about 5 minutes, whereas prostigmine made a long lasting significant enlargment of the amplitudes of peristalsis without any modification of intraluminal pressure. Serum gastrin levels increased after application of PGE2 and PGF2 alpha and remained constant after prostigmine. A possible way of action of PG's in the gastrointestinal tract is discussed, based on experiments concerning PG-application after different periods of time.

Topics: Acute Disease; Animals; Gastrins; Gastrointestinal Motility; Intestinal Obstruction; Manometry; Prostaglandins; Rabbits

Topics: Acetylcholine; Acute Disease; Amides; Amino Acids; Animals; Bethanechol Compounds; Blood Pressure; Chronic Disease; Dogs; Drug Synergism; Gastric Fistula; Gastric Juice; Gastrins; Gastrointestinal Motility; Guinea Pigs; Histamine; Ileum; Male; Methacholine Compounds; Pepsin A; Peptides; Perfusion; Pylorus; Rats; Stomach; Tachyphylaxis