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YEGEN, ŞEVKET CUMHUR

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YEGEN

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ŞEVKET CUMHUR

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1999 - 20002
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Author: YEGEN, BERRAK × Subject: CELLS ×

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    Role of nitric oxide in gastric injury induced by hemorrhagic shock in rats
    (KARGER, 2000) DENİZBAŞI ALTINOK, ARZU; Denizbasi, A; Yegen, C; Ozturk, M; Yegen, B
    The aim of this study was to investigate the effect of nitric oxide (NO) on the gastric injury induced by hemorrhagic shock. Hemorrhagic shock was created by withdrawing 3 ml blood/200 g body weight of the rats. Before the hemorrhage, N-G-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v. bolus), D-NAME (10 mg/kg i.v. bolus), or L-arginine (100 mg/kg i.v. bolus and 10 mg/kg/min infusion) + L-NAME were administered. At the end of the 1-hour hypovolemic shock period, histological analysis, gastric ulcer index, gastric myeloperoxidase (MPO) activity, and gastric protein oxidation (PO) levels were determined. In histological analysis a destructive effect of L-NAME (NO synthase inhibitor) was demonstrated. L-NAME treatment increased gastric MPO activity, L-arginine reversed this effect and D-NAME had no effect. Tissue PO activity was found to be increased in L-NAME-treated rats; L-arginine treatment reversed this activity. It is concluded that gastric barrier function is altered after hemorrhagic shock, and L-arginine (NO precursor) can prevent mucosal injury in the stomach. This effect of NO may be on gastric blood flow and can be mediated by tissue neutrophils. Copyright (C) 2000 S. Karger AG, Basel.
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    Role of endothelins in trinitrobenzene sulfonic acid-induced colitis in rats
    (KARGER, 1999) YEGEN, BERRAK; Gulluoglu, B; Kurtel, H; Gulluoglu, MG; Yegen, C; Aktan, AO; Dizdaroglu, F; Yalin, R; Yegen, BC
    To determine the role of endothelins (ET) on experimental colitis, following intracolonic trinitrobenzene sulfonic acid administration, rats were given orally either bosentan (BS), a nonselective ET receptor antagonist (100 mg/kg in 5% arabic gum), or arabic gum by gavage for 2 or 14 days. Macroscopic damage scores obtained in the vehicle (1.4 +/- 0.4), acute (4.8 +/- 0.6) and chronic (3.8 +/- 0.3) colitis groups were significantly higher than in the control group (0). BS treatment reduced the scores in both acute (3 +/- 0.5) and chronic (2.3 +/- 0.5) colitis groups. Myeloperoxidase (MPO) activities of colonic tissues were elevated in acute and chronic colitis groups (325.1 +/- 44.9 and 431.8 +/- 54.6 U/g wet weight) as compared with the control group (73.6 +/- 11 U/g wet weight). Plasma protein oxidation levels were found to be significantly increased in the chronic colitis group (1,158.1 +/- 63.4 nmol/ml) compared with the control, ethanol and acute colitis groups (274.3 +/- 23.1, 490 +/- 52.2 and 422.2 +/- 50.5 nmol/ml). BS treatment significantly reduced both the protein oxidation level (375.5 +/- 46.9 nmol/ml) and MPO activity (167.5 +/- 35.8 U/g wet weight). The results of the present study suggest the involvement of ETs in the pathogenesis of colonic injury in this animal model of colitis.