Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various blood flow disturbances in intraabdominal digestive organs were studied clinically and experimentally from a viewpoint of vascular surgery. Acute gastric mucosal lesion may occur due to ischemia and reperfusion injury of the gastric mucosa. Bleeding from stomach ulcer may be rarely caused by consumption coagulopathy along with aortic aneurysm. Heparin therapy was successful to interrupt it. Gastrectomy is not indicated for such condition but aneurysm should be repaired. Portal vein reconstruction for the radical resection of hepatic, biliary and pancreatic cancers should be carefully made, because early or late stenosis occurs frequently, and they may connect to early or late morbidities or mortalities. On the other hand, resection and replacement of the suprarenal vena cava invaded by the retroperitoneal malignant tumor may be safely carried out. For the acute mesenteric arterial occlusion, early diagnosis and arterial reconstruction are essential to save catastrophe. Positive Doppler sound on the vasa recta seems to be the most reliable parameter for assessing bowel viability. Approach from the proximal large arteries is recommended for uncontrollable intraperitoneal bleeding.
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PMID:[Blood flow disturbance in digestive organs--a viewpoint of vascular surgery]. 258 8

The healing effect of heparin on gastric ulcer and its underlying mechanisms were studied. The influences of protamine on these effects were also investigated. Gastric ulcer was induced by acetic acid in rats. Heparin (100-1000 U/kg i.v.) was given once daily for 4 or 7 days. Ulcer area was measured; gastric mucosal regeneration, proliferation, and angiogenesis were determined by histological or immunohistochemical methods. Gastric mucosal basic fibroblast growth factor (bFGF) level was assessed by an enzyme-linked immunosorbent assay, and the mucosal epidermal growth factor (EGF) level and nitric oxide synthase (NOS) activity were measured by radioimmunoassay. The anticoagulant action of heparin was determined by the duration of bleeding time. The results showed that heparin given for 4 or 7 days significantly accelerated gastric ulcer healing in a dose-dependent manner. The three doses of heparin significantly stimulated mucosal regeneration and proliferation as well as angiogenesis but not the contraction of ulcer base. Similar effects were observed in gastric mucosal bFGF and EGF levels and constitutive NOS activity. Protamine not only abolished the anticoagulant action of heparin but also significantly potentiated its effects on ulcer healing, gastric mucosal proliferation, angiogenesis, and constitutive NOS activity. These findings indicate that heparin can accelerate gastric ulcer healing, which is associated with mucosal regeneration, proliferation, and angiogenesis. These actions are likely to be stimulated by bFGF, EGF, and constitutive NOS activity in the gastric mucosa. Protamine potentiates the ulcer-healing effect of heparin, which is probably acting through constitutive NOS activation.
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PMID:Association of heparin with basic fibroblast growth factor, epidermal growth factor, and constitutive nitric oxide synthase on healing of gastric ulcer in rats. 1041 93

Our preliminary finding indicated that intravenous (i.v.) injection of heparin increased gastric ulcer healing in rats. However, the anticoagulant action of i.v. heparin could produce complications in ulcer patients if the drug was used as an anti-ulcer agent. The present study aimed to investigate whether intragastric (i.g.) administration of heparin, known to have no anticoagulant activity, would have the similar ulcer healing effect and the relationship of this effect, if any, with nitric oxide (NO), a substance suggested to be important for ulcer healing. Heparin (100, 500, 1000 U/kg, i.g. ) administered once daily for 4 days accelerated the healing of gastric ulcer induced by acetic acid in Sprague-Dawley rats, which was accompanied by an increase in mucosal proliferation and regeneration at the ulcer margin, microvessel number both at the ulcer margin and base, and the thickness of mucus layer. Both activity and content, but not the mRNA of constitutive nitric oxide synthase (cNOS) in the gastric mucosa were enhanced. L-N(G)-nitroarginine methyl ester (L-NAME), an inhibitor of NOS activity blocked the cNOS activity activated by heparin and reversed the beneficial effects of heparin on ulcer healing. The bleeding time was not altered by i.g. heparin. These findings demonstrate that i.g. heparin promotes the healing processes of gastric ulcer. Such effect is suggested to act through the stimulation of mucosal cNOS activity. In addition, i.g. heparin is better than i.v. heparin without the potential anticoagulation effect.
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PMID:Intragastric administration of heparin enhances gastric ulcer healing through a nitric oxide-dependent mechanism in rats. 1088 21