fibrin and Stomach-Ulcer

The interaction of antithrombin (AT) with cell surface glycosaminoglycans has been shown to promote the endothelial release of prostacyclin (PGI2). Because PGI2 plays an important role in gastric cytoprotection, we examined whether AT prevents water-immersion restraint stress (WIR)-induced gastric mucosal injury in rats by promoting the endothelial release of PGI2. Intravenous administration of AT (250 U/kg) prevented WIR-induced gastric mucosal injury in rats. Gastric levels of 6-keto-prostaglandin F1alpha, a stable metabolite of PGI2, were significantly increased 0.5 and 1 hour after WIR in animals administered AT compared with control animals. The effects induced by AT in animals subjected to WIR were not observed in animals that were administered DEGR-Xa, a selective inhibitor of thrombin generation, or Trp49-modified AT, which lacks affinity for heparin. In animals subjected to WIR gastric mucosal blood flow was significantly reduced with a simultaneous increase in gastric mucosal microvascular permeability. Activated neutrophils have been implicated in the WIR-induced reduction of gastric mucosal blood flow by increasing microvascular permeability. Although AT prevented the reduction of gastric mucosal blood flow and the increase in gastric mucosal microvascular permeability in animals subjected to WIR, neither DEGR-Xa nor Trp49-modified AT had any effect. Pretreatment of animals with indomethacin completely inhibited the protective effects of AT against WIR-induced gastric mucosal injury and the AT-induced increase in post-WIR gastric 6-keto-prostaglandin F1alpha levels. These results strongly suggest that AT prevents stress-induced gastric mucosal injury by increasing the gastric levels of PGI2 through the interaction of AT with cell-surface glycosaminoglycans, thus increasing gastric mucosal blood flow both by vasodilation and by inhibiting neutrophil activation.

Topics: 6-Ketoprostaglandin F1 alpha; Albumins; Amino Acid Chloromethyl Ketones; Animals; Anti-Inflammatory Agents, Non-Steroidal; Antithrombins; Epoprostenol; Factor Xa; Fibrin; Fibrinogen; Gastric Mucosa; Immersion; Indomethacin; Male; Peroxidase; Rats; Rats, Wistar; Regional Blood Flow; Stomach Ulcer; Stress, Physiological; Time Factors; Tryptophan

Endoscopic injection therapy is a well established method of controlling peptic ulcer haemorrhage but the optimum injection solution and the mechanism involved in inducing haemostasis are unknown.. The efficacy and effects on tissue of various therapeutic agents used in the control of gastric mucosal haemorrhage were studied in ten rabbits. Thirty-eight bleeding mucosal ulcers (blood loss above 1.5 ml/min) created at gastrotomy were studied. Adrenaline (1:100,000), thrombin, fibrin (thrombin plus fibrinogen), 5 per cent ethanolamine and 50 per cent dextrose were injected; a fibrin suspension was also sprayed around bleeding ulcers.. Sclerosants were found to be least effective in the control of bleeding and were associated with significant tissue necrosis. Although all the other solutions significantly decreased blood loss within 30 min of injection (median blood loss 0.25 ml/min), only an injected mixture of adrenaline plus thrombin and sprayed fibrin achieved complete haemostasis within 2 min of treatment and with no recurrence of bleeding. Neither agent caused significant tissue damage. Histological examination showed that no solution caused arterial thrombosis when injected next to a major ear artery.. Sclerosants caused extensive tissue necrosis and were least effective in the control of ulcer haemorrhage. A combination of dilute adrenaline and human thrombin may represent optimal haemostatic therapy for peptic ulcer haemorrhage.

Topics: Animals; Epinephrine; Ethanol; Fibrin; Gastrointestinal Hemorrhage; Glucose; Hemostasis; Injections; Rabbits; Stomach Ulcer; Thrombin

The stomach surgically removed from 38 patients because of chronic ulcers are studied. The fibrinoid necrosis zone observed at the bottom of 30 ulcers is formed of two layers out of which the superficial layer only is necrotic while the deep one represent a fibrinoid swelling. The latter consists of the network of collagen fibers and fibrin elements with surviving connective tissue cells. Two processes going into the opposite directions take place on the border between the fibrinoid zone and granulation tissue: the spread of the fibrinoid to the granulation tissue and its organization by the granulation tissue elements. Interrelationship between these processes as well as the intensity of the fibrinoid necrosis rejection from the surface determines the thickness of the zone. Fibrinoid prevents the stomach wall digestion but at the same time inhibits the ulcer healing.

Topics: Adult; Chronic Disease; Fibrin; Gastrectomy; Gastric Mucosa; Histocytochemistry; Humans; Microscopy, Electron; Middle Aged; Necrosis; Staining and Labeling; Stomach; Stomach Ulcer

Topics: Animals; Cell Aggregation; Fibrin; Gastric Mucosa; Granulation Tissue; Guinea Pigs; Histamine; Leukocytes; Male; Necrosis; Periodic Acid; Promethazine; Regeneration; Staining and Labeling; Stomach Ulcer; Time Factors

Topics: Cicatrix; Epithelial Cells; Fibrin; Gastric Juice; Gastric Mucosa; Granulation Tissue; Humans; Necrosis; Peptic Ulcer Perforation; Stomach Ulcer

Topics: Arthritis, Rheumatoid; Female; Fibrin; Histocytochemistry; Humans; Male; Necrosis; Placenta; Rheumatoid Nodule; Stomach Ulcer; Synovial Membrane

Topics: Blood Cell Count; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Duodenal Ulcer; Fibrin; Fibrinolysis; Heparin Antagonists; Humans; Postoperative Complications; Solubility; Stomach Ulcer; Wound Healing

Topics: Arteriosclerosis Obliterans; Arteritis; Biomedical Research; Celiac Artery; Fibrin; Gastrectomy; Glycosaminoglycans; Humans; Sclerosis; Stomach Ulcer; Takayasu Arteritis; Thromboangiitis Obliterans; Ulcer