pituitrin and Stomach-Ulcer

Stress ulcers are multiple superficial mucosal lesions which occur mainly in the fundus of stomachs of seriously ill patients and should be differentiated from reactivation of a pre-existent ulcer diathesis, Cushing's ulcer following head injury, or drug-induced gastritis. It is generally agreed that luminal acid and pepsin are required for ulceration to develop. Experimental evidence suggests that backdiffusion of acid is closely related to the formation of ulcers. In the absence of overt disruption of the gastric mucosal barrier, ischaemia appears to compromise the ability of the gastric mucosa to dispose of backdiffusing acid, which then results in a decrease in intramural pH and ulceration. Reflux of duodenal contents and diffusion of urea from the blood may contribute to the formation of ulcers. Although endoscopic studies have demonstrated gross mucosal injury within hours of the stressful event in nearly 100 per cent of patients examined, most stress ulcers heal when normal gastric defence mechanisms are restored. However, in a small percentage of patients, stress ulceration may lead to frank gastrointestinal haemorrhage requiring medical and/or surgical intervention. Endoscopic findings in conjunction with the history usually differentiates stress ulcer from other bleeding lesions. Angiography may be used if endoscopy fails to identify the bleeding site. Most episodes of bleeding from stress ulceration resolve on medical management consisting of saline lavage, antacids, and adequate supportive measures. Pharmacoangiography with selective infusion of vasopressin or embolization may be of benefit in selected patients with continued bleeding. Surgery is a last resort and has a predictably high mortality. The operation of choice is controversial, but vagotomy, pyloroplasty and oversewing the ulcers may be a good initial operation. Continued bleeding subsequent to vagotomy and pyloroplasty would require near total gastrectomy. Since results of surgical therapy in established stress ulcer disease are poor, the prevention of bleeding is the most rational approach to the management of this disease. The key to prophylaxis is the maintenance of normal intragastric pH. Antacids appear to be superior to cimetidine in preventing bleeding from stress ulcers, so long as the gastric content is buffered to a pH of 3.5 or greater. In seriously ill patients found in respiratory-surgical intensive care units, hourly titration with antacids is the standard against whi

Topics: Antacids; Cimetidine; Endoscopy; Gastrectomy; Gastric Acid; Gastric Mucosa; Humans; Hydrogen-Ion Concentration; Pepsin A; Peptic Ulcer Hemorrhage; Regional Blood Flow; Stomach Ulcer; Stress, Psychological; Vasopressins

Topics: Acute Disease; Animals; Duodenal Ulcer; Gastrectomy; Gastric Mucosa; Gastritis; Gastroscopy; Humans; Intestinal Mucosa; Peptic Ulcer; Peptic Ulcer Hemorrhage; Permeability; Stomach Ulcer; Stress, Psychological; Vagotomy; Vasopressins

Topics: Abdomen; Aged; Crohn Disease; Duodenal Diseases; Duodenal Ulcer; Esophageal Achalasia; Esophagitis; Follow-Up Studies; Gastrectomy; Gastritis; Gastrointestinal Hemorrhage; Hematoma; Hernia, Diaphragmatic; Humans; Intestine, Small; Methods; Obesity; Peptic Ulcer Hemorrhage; Postoperative Complications; Stomach Neoplasms; Stomach Ulcer; Vagotomy; Vasopressins; Zollinger-Ellison Syndrome

Topics: Cimetidine; Clinical Trials as Topic; Emergencies; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hemostatic Techniques; Humans; Peptic Ulcer; Peptic Ulcer Hemorrhage; Stomach Ulcer; Stress, Physiological; Vasopressins

The high prevalence of gastric ulceration underlines the importance of understanding the mechanisms. Based upon its multifactorial role vasopressin (VP) is supposed to be one of the contributory factors, however the data are contradictory. We intended to reevaluate the role of VP in development of gastric ulceration. Naturally VP-deficient Brattleboro rats were used and the indomethacine-induced gastric erosion model (35 mg/kg sc, 4 h) has been chosen because of its clinical importance. Since gastric mucosal vulnerability shows age-dependent alterations, we compared young (4 week old) rats to old ones (1 year old). The lack of VP resulted in attenuation of erosion formation in young rats, while aggravation in old ones. Four hours after indomethacin treatment adrenocorticotropin and corticosterone levels as well as blood glucose levels were higher in VP-deficient rats, independent of the age. Old VP-deficient Brattleboro rats had smaller thymuses. Our results demonstrate the age-dependent role of VP in susceptibility of gastric mucosa to indomethacin-induced injury. Probably the absence of VP per se is not the reason of the data obtained but also the hormonal and metabolic consequences of VP deficiency (e.g. short versus long-term corticosterone and blood glucose elevation as well as related immunodisturbances).

Topics: Adrenocorticotropic Hormone; Aging; Animals; Blood Glucose; Corticosterone; Female; Gastric Mucosa; Indomethacin; Male; Rats; Rats, Mutant Strains; Stomach Ulcer; Vasopressins

Since endogenous vasopressin has been reported to be an aggressor in the gastric mucosa and a vasoconstrictor in the gastric circulation, we investigated the gastric cytoprotective effects of OPC-21268, a newly developed, nonpeptide, orally active vasopressin-1 receptor antagonist, on ethanol-induced gastric injury in rats. The rats were treated with OPC-21268 or placebo 2 hr before ethanol administration, and the gastric mucosa was evaluated macroscopically for ulcer damage, and histologically for gastric mucosal injury. Gastric mucosal blood flow, erythrocyte volume, and erythrocyte velocity were also measured in groups given saline, ethanol alone, and ethanol after OPC-21268. To investigate the role of systemic or locally secreted vasopressin, we measured plasma and tissue (gastric mucosa) vasopressin concentrations after ethanol or vehicle administration. Prophylactic OPC-21268 treatment improved the gastric ulcer score in a dose-dependent manner, and histological examination demonstrated that the drug significantly ameliorated the gastric injury induced by ethanol. The hemodynamic values obtained in the OPC-21268-treated and ethanol-treated group were similar to those in the saline control group, but values were significantly (P < 0.05) higher for gastric mucosal blood flow and erythrocyte velocity and lower for erythrocyte volume compared to the group given ethanol alone. Plasma vasopressin concentrations were not significantly different in the control group and at 15, 30, and 60 min after administration of ethanol. However, ethanol administration caused a threefold increase in gastric tissue vasopressin level (P < 0.05) compared to the control group. These results suggested that OPC-21268 relieved congestive hyperemia in the gastric mucosa and ameliorated the mucosal injury caused by ethanol, probably as a result of inhibition of vasopressin-mediated actions on the stomach. The vasopressin involved was probably generated locally in the gastric mucosa after ethanol administration.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Ethanol; Gastric Mucosa; Male; Microcirculation; Piperidines; Quinolones; Rats; Stomach Ulcer; Vasopressins

Topics: Adrenocorticotropic Hormone; Animals; Arginine Vasopressin; Brain; Diabetes Insipidus; Immersion; Injections, Intraventricular; Male; Rats; Rats, Inbred Strains; Stomach Ulcer; Stress, Physiological; Vasopressins

The effects of different doses of Asu(1,7) eel-calcitonin, peripherally injected, on gastric secretion were studied in conscious Brattleboro rats, which are genetically deficient in vasopressin. Moreover, we evaluated the activity of this analogue on gastric ulcer formation by restraint stress. We found that 5 IU/kg Asu(1,7) eel-calcitonin decreased gastric secretion and inhibited the development of stress-induced ulcers in Brattleboro rats. These data suggest that vasopressin does not play a role in the gastrointestinal activity of Asu(1,7) eel-calcitonin.

Topics: Animals; Calcitonin; Eels; Gastric Mucosa; Heterozygote; Homozygote; Injections, Intravenous; Male; Rats; Rats, Brattleboro; Reference Values; Stomach Ulcer; Stress, Physiological; Vasopressins

Stress ulcers are located in the body and fundic part of the stomach. They occur in the majority of severely ill or injured patients, but only about 10% will bleed. The most effective prophylaxis are measures against the condition giving rise to risk factors as septicaemia, shock and malnutrition. The medical prophylaxis consists of antacids and/or histamine2-blockers. Most bleedings will stop after intensive care and medication with vasopressin particularly if risk factors can be eliminated. Gastric surgery should be the last step in the treatment of bleeding stress ulcers and then we recommend non-resectional surgery as gastric devascularisation or suture ligation of bleeding vessels.

Topics: Antacids; Histamine H2 Antagonists; Humans; Peptic Ulcer Hemorrhage; Stomach Ulcer; Stress, Physiological; Vasopressins

Since bleeding from acute lesions of the gastric mucosa can cease spontaneously and the mortality rate of emergency surgery is high, conservative treatment is always preferable. Satisfactory results were obtained with continuous infusions of vasopressin in low doses (0.2 U/kg/hr for 8 hours) so that this treatment appears a valid alternative to more recent techniques (somatostatin).

Topics: Acute Disease; Adult; Aged; Female; Gastritis; Gastrointestinal Hemorrhage; Humans; Infusions, Intra-Arterial; Male; Middle Aged; Peptic Ulcer Hemorrhage; Radiography; Stomach Ulcer; Vasopressins

Susceptibility to ulceration induced by restraint, restraint plus intermittent shock, and activity stress was studied in 6 week and 18 week old Brattleboro and Long-Evans rats. Older animals developed more glandular ulcers than younger animals with Brattleboro rats having significantly greater ulceration than Long-Evans rats in both conditions. With activity stress, younger subjects developed significantly more glandular ulcers than older subjects; whereas, older subjects developed significantly more nonglandular ulcers than younger subjects. In both instances, the ulceration was significantly greater in Brattleboro rats than in Long-Evans rats. There were significantly high correlations among running behavior, survival time, and the development of glandular ulcers in younger animals exposed to activity stress. The presence of vasopressin, as well as the age of the subject and the nature of the stress, influences the type and degree of stomach pathology induced.

Topics: Aging; Animals; Diabetes Insipidus; Electroshock; Male; Motor Activity; Rats; Rats, Brattleboro; Rats, Inbred Strains; Restraint, Physical; Species Specificity; Stomach Ulcer; Stress, Psychological; Vasopressins

Topics: Acidosis; Anti-Ulcer Agents; Blood Coagulation Disorders; Enteral Nutrition; Humans; Intensive Care Units; Intubation, Gastrointestinal; Peptic Ulcer Hemorrhage; Plasma Substitutes; Somatostatin; Stomach Ulcer; Stress, Physiological; Vasopressins

Topics: Anti-Ulcer Agents; Gastric Mucosa; Gastritis; Gastrointestinal Hemorrhage; Humans; Peptic Ulcer Hemorrhage; Prostaglandins; Somatostatin; Stomach Ulcer; Stress, Physiological; Vasopressins

The effect of barrier breakers on gastric mucosal blood flow (MBF) has been disputed, but the influence of acid back diffusion alone has never been studied. In anesthetized New Zealand white rabbits, intramural pH (pHi) and gastric MBF were measured with an antimony microelectrode and with radioactive microspheres (51Cr, 85Cr, 141Ce), respectively. Innervated fundic pouches were perfused with solutions of varying [H+] at 37 degrees C. In the rabbit, back flux of H+ is linearly dependent on luminal [H+] and in the present studies a direct positive linear correlation was found between luminal [H+] and MBF (r = 0.97 P < 0.001) while pHi remained unchanged up to luminal [H+] of 80 mM. The usual 80% increase in MBF induced by 80 mM HCl was prevented by pretreatment with vasopressin, which decreased pHi and caused gross ulceration. Without vasopressin, [H+] of 120 mM HCl produced gross mucosal ulceration and a decrease in MBF and pHi. Our data suggest that back diffusion of H+ influences MBF in the rabbit. There is an increasing MBF caused by increasing luminal [H+] up to 80 mM, beyond which MBF decreases. When the balance between back diffusion and MBF is disturbed by a vasoconstrictor or a high luminal [H+], pHi decreases and gross ulceration occurs.

Topics: Animals; Buffers; Diffusion; Gastric Fundus; Gastric Mucosa; Hydrogen; Hydrogen-Ion Concentration; Ions; Perfusion; Rabbits; Regional Blood Flow; Stimulation, Chemical; Stomach Ulcer; Vasopressins

Topics: Acute Disease; Adult; Aged; Diverticulum, Colon; Duodenal Ulcer; Gastritis; Gastrointestinal Hemorrhage; Humans; Infusions, Intra-Arterial; Mallory-Weiss Syndrome; Middle Aged; Peptic Ulcer Hemorrhage; Radiography; Stomach; Stomach Ulcer; Varicose Veins; Vasopressins

The influence of various ulcerogenic treatments on healing gastric ulcers induced by thermocautery was studied in mice. A low dose of serotonin (5HT) which did not produce ulceration, was found to aggravate gastric ulcers at 15th or 30th day after thermocauterization, but other ulcerogenic treatments including histamine, norepinephrine, vasopressin, acetic acid ingestion and cold-restraint stress did not affect this induced gastric ulcer. Bleeding and ulceration, however, occurred in the gastric glandular portion in addition to thermocauterization ulcer by the treatment of acetic acid ingestion or cold-restraint stress. Histological sections of gastric ulcers (15th and 30th day) 24 hr after 5HT injection, showed severe necrosis of the regenerated mucosal layer. Microvessel structure in the gastric mucosa as revealed by the Indian-ink infusion, showed a local obstruction of blood flow on the edge of ulcers 1 or 3 hr after 5HT injection. Although acetic acid ingestion increased transmucosal fluxes of Na+ and K+, 5HT had no effect on the ion flux in normal mice. Thus the healed ulcer area was resistant to various ulcerogenic stimulants, except for 5HT, and the vasoactive factor of 5HT may be involved in the aggravating process of gastric ulcers induced by thermocautery.

Topics: Acetates; Animals; Gastric Mucosa; Histamine; Hot Temperature; Ions; Male; Mice; Norepinephrine; Potassium; Regeneration; Serotonin; Sodium; Stomach Ulcer; Vasopressins

Aggressive treatment with H(2) receptor blocking agents and/or antacids has been advocated as effective prophylaxis against and treatment for "stress ulcer," based on the logical but infrequently tested assumption that the severity of the disease is critically determined by the concentration of intraluminal acid. The present study investigated this assumption in a model which employed topical acid, topical bile acid and mucosal ischemia to induce ulcerogenesis. With vascularized, chambered ex vivo wedges of canine proximal gastric wall, groups of animals were studied during three sequential periods using topical test solutions (TS) containing either 0 mM, 100 mM or 160 mM HCI. During period 1, mucosae were exposed to TS alone; during period 2, either to TS containing 1 mM sodium taurocholate (TC) or to TS and concomitant vasopressin infusion (VP); and during period 3, to TS + TC + VP. Parameters evaluated included net H(+) flux ( big up tri, openH(+)), aminopyrine clearance (AC), a measure of mucosal blood flow, net TC flux ( big up tri, openTC) and the lesion index, graded 0-5. The data indicate that in nonischemic mucosa exposed to constant [TC], AC was significantly increased, big up tri, openH(+) ("back-diffusion") increased as a linear function of [H(+)] and no lesions were observed. Under the same circumstances in ischemic mucosa, big up tri, openH(+) increased as linear function of [H(+)]. As a consequence, lesion severity was also a linear function of [H(+)]. big up tri, openTC was enhanced at low pH but bore no relation to the degree of mucosal damage induced. Assuming applicability of the model, these studies provide support for the use of H(2) receptor blocking agents and/or antacids to prevent or ameliorate "stress ulcer" disease.

Topics: Acute Disease; Administration, Topical; Aminopyrine; Animals; Bile Acids and Salts; Disease Models, Animal; Dogs; Female; Gastric Mucosa; Humans; Hydrogen-Ion Concentration; Ischemia; Male; Stomach Ulcer; Stress, Psychological; Taurocholic Acid; Vasopressins

Topics: Angiography; Embolization, Therapeutic; Endoscopy; Gastrointestinal Hemorrhage; Humans; Hydrogen-Ion Concentration; Peptic Ulcer Hemorrhage; Postoperative Complications; Stomach Ulcer; Stress, Physiological; Vasopressins

Topics: Acute Disease; Administration, Topical; Aminopyrine; Animals; Bile Acids and Salts; Dogs; Gastric Mucosa; Hydrogen; Ischemia; Methylprednisolone; Sodium; Stomach Ulcer; Vasopressins

An ulcer was induced in the anterior wall of the antrum by local injection of acetic acid solution. Carbonized microspheres 15 +/- 5 micrometer in diameter, labeled with 85Sr and 141Ce, were used to measure blood flow in different regions and layers of the stomach wall, and in each sample the mucosa was separated from the muscularis. The radioactivity of a blood reference sample and the tissue sample was determined, and the blood flow was calculated for each tissue sample. Two groups of anesthetized animals were used: animals with normal stomachs given vasopressin and animals with a 1-week ulcer given vasopressin. The vasopressin was administered intravenously over a 20-min period. In animals with normal stomachs and in animals with a gastric ulcer vasopressin was found to decrease the blood flow to the stomach in all areas examined. The presence of a 1-week ulcer in the cat did not seem to influence the effect of vasopressin.

Topics: Animals; Cats; Female; Gastric Mucosa; Male; Microspheres; Regional Blood Flow; Stomach; Stomach Ulcer; Vasopressins

Topics: Angiography; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Injections, Intra-Arterial; Liver Cirrhosis; Peptic Ulcer Hemorrhage; Stomach Ulcer; Vasopressins

Topics: Animals; Antacids; Burns; Central Nervous System Diseases; Humans; Peptic Ulcer; Postoperative Complications; Stomach Ulcer; Stress, Physiological; Vasopressins; Wounds and Injuries

Two patients developed spontaneous bacterial peritonitis after infusions of vasopressin into the superior mesenteric or gastroduodenal arteries for upper gastrointestinal hemorrhage. The peritonitis in these patients differed from the typical picture in which a single aerobic organism is responsible, by the presence of multiple organisms, some of which were anaerobic. These findings suggest that the arterial vasoconstriction decreased the integrity of the intestinal mucosal barrier and permitted the transmural migration of enteric organisms from the lumen of the bowel into the ascites-filled peritoneal cavity.

Topics: Anaerobiosis; Arteries; Ascitic Fluid; Bacterial Infections; Duodenum; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Infusions, Parenteral; Intestines; Male; Mesenteric Arteries; Middle Aged; Peritonitis; Stomach; Stomach Ulcer; Vasopressins

Topics: Blood Transfusion; Esophageal Diseases; Gastrointestinal Hemorrhage; Humans; Injections, Intra-Arterial; Liver Cirrhosis; Peptic Ulcer Hemorrhage; Recurrence; Stomach Ulcer; Varicose Veins; Vasopressins

Topics: Animals; Bile; Bile Acids and Salts; Disease Models, Animal; Dogs; Gastric Juice; Gastric Mucosa; Gastritis; Gastrointestinal Hemorrhage; Humans; Hydrogen-Ion Concentration; Ischemia; Peptic Ulcer Hemorrhage; Secretory Rate; Stomach Ulcer; Vasopressins

A bleeding gastric ulcer was surgically created in 18 dogs, and the left gastric artery was successfully catheterized by percutaneous techniques in 15. Nine of these dogs were treated with vasopressin infusion which did not arrest the hemorrhage. A total of 11 dogs (five of them following unsuccessful vasopressin therapy) underwent embolization with strips of Gelfoam, and hemorrhage stopped in ten. This technique of embolization is concluded to be of value in the management of gastric hemorrhage.

Topics: Angiography; Animals; Arteries; Catheterization; Celiac Artery; Contrast Media; Dogs; Embolism; Gastrointestinal Hemorrhage; Gelatin Sponge, Absorbable; Stomach; Stomach Ulcer; Vasopressins

Superior mesenteric arteriography can often demonstrate actively bleeding marginal ulcers. Five cases diagnosed by angiography are reported. Pitressin infusions of the superior mesenteric artery stopped bleeding permanently in two cases, transiently in two cases, and was not attempted in one case. Pitressin infusions of the superior mesenteric artery should be attempted before surgery is performed for bleeding marginal ulcers.

Topics: Adult; Aged; Angiography; Catheterization; Female; Humans; Infusions, Parenteral; Male; Middle Aged; Peptic Ulcer; Peptic Ulcer Hemorrhage; Stomach Ulcer; Vasopressins

Topics: Animals; Atropine; Autonomic Agents; Chlorpromazine; Dibenzylchlorethamine; Gastric Juice; Gastric Mucosa; Isoproterenol; Male; Papaverine; Pentobarbital; Phenoxybenzamine; Pigments, Biological; Propranolol; Rats; Regional Blood Flow; Scopolamine; Stomach; Stomach Ulcer; Stress, Physiological; Tetraethylammonium Compounds; Vasopressins

Topics: Antacids; Diagnosis, Differential; Humans; Stomach Ulcer; Stress, Physiological; Ulcer; Vasopressins; Wounds and Injuries

Topics: Animals; Dogs; Gastric Acidity Determination; Gastric Mucosa; Membrane Potentials; Stomach Ulcer; Taurocholic Acid; Vasopressins

Topics: Acute Disease; Duodenal Ulcer; Epinephrine; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Portography; Stomach Ulcer; Vasopressins

Topics: Animals; Ischemia; Norepinephrine; Rats; Stomach; Stomach Ulcer; Stress, Physiological; Sympathetic Nervous System; Vasopressins

Topics: Animals; Bethanechol Compounds; Cholecystokinin; Female; Glucagon; Humans; Pancreatic Cyst; Pancreatic Diseases; Pancreatic Neoplasms; Pancreatitis; Propantheline; Radioisotopes; Radionuclide Imaging; Rats; Selenium; Stomach Ulcer; Vasopressins

Topics: Acetylcholine; Amine Oxidase (Copper-Containing); Analysis of Variance; Animals; Autonomic Agents; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Glucose; Histamine; Histamine Release; Humans; Insulin; Methods; Pentagastrin; Pepsin A; Rats; Reserpine; Secretory Rate; Stomach; Stomach Ulcer; Vasopressins

Topics: Aged; Angiography; Blood Transfusion, Autologous; Humans; Intubation, Gastrointestinal; Ischemia; Male; Necrosis; Peptic Ulcer Hemorrhage; Stomach; Stomach Diseases; Stomach Ulcer; Vasopressins

Topics: Aminopyrine; Animals; Bethanechol Compounds; Blood Pressure; Diffusion; Dogs; Gastric Mucosa; Hemorrhage; Histamine; Hydrochloric Acid; Injections, Intravenous; Ischemia; Norepinephrine; Pentagastrin; Sodium Chloride; Stomach Ulcer; Time Factors; Vasopressins

Topics: Aged; Angiography; Epinephrine; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Peptic Ulcer Hemorrhage; Propranolol; Stomach Ulcer; Vasopressins

Topics: Angiography; Celiac Artery; Duodenal Ulcer; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Injections, Intra-Arterial; Liver Cirrhosis; Mesenteric Arteries; Peptic Ulcer Hemorrhage; Stomach Ulcer; Vasopressins

Topics: Adult; Aged; Arteries; Capillaries; Celiac Artery; Colonic Diseases; Diverticulum, Colon; Duodenal Ulcer; Epinephrine; Gastritis; Gastrointestinal Hemorrhage; Hernia, Diaphragmatic; Humans; Infusions, Parenteral; Male; Mallory-Weiss Syndrome; Mesenteric Arteries; Middle Aged; Peptic Ulcer Hemorrhage; Radiography; Stomach Ulcer; Vasopressins

Topics: Angiotensin II; Animals; Blood Circulation; Blood Pressure; Clonidine; Cold Temperature; Drug Synergism; Gastric Juice; Gastric Mucosa; Gastrointestinal Hemorrhage; Immobilization; Male; Norepinephrine; Rats; Secretory Rate; Stomach Ulcer; Stress, Physiological; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Topics: Aminocaproates; Blood Coagulation Disorders; Blood Transfusion; Duodenal Ulcer; Esophageal and Gastric Varices; Esophagitis; Fibrinogen; Fibrinolysis; Gastritis; Gastrointestinal Hemorrhage; Heparin; Humans; Liver Diseases; Phosphorus Isotopes; Portacaval Shunt, Surgical; Stomach Ulcer; Therapeutic Irrigation; Vasopressins; Vitamin K

Topics: Acute Disease; Adult; Aged; Alcoholism; Animals; Colitis; Colitis, Ulcerative; Diverticulum, Colon; Dogs; Epinephrine; Female; Gastrointestinal Hemorrhage; Humans; Ileitis; Injections, Intra-Arterial; Male; Mesenteric Arteries; Middle Aged; Peptic Ulcer Hemorrhage; Propranolol; Regional Blood Flow; Stomach Ulcer; Vasoconstrictor Agents; Vasopressins

Topics: Angiography; Animals; Felypressin; Gastric Mucosa; Guinea Pigs; Histamine; Male; Regional Blood Flow; Stomach Ulcer; Vasopressins

Topics: Animals; Dogs; Histamine; Histamine Agents; Peptic Ulcer; Stomach Ulcer; Vasopressins