Person: DAĞLI, EMRULLAH TOLGA
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DAĞLI
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EMRULLAH TOLGA
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Publication Metadata only Oxygen radicals and nitric oxide in rat mesenteric ischaemia-reperfusion: Modulation by L-arginine and N-G-nitro-L-arginine methyl ester(WILEY, 1998) YALÇIN, AHMET SUHA; Haklar, G; Ulukaya-Durakbasa, C; Yuksel, M; Dagli, T; Yalcin, AS1. The aims of the present study were to detect changes in superoxide anion (O-2(.-)), nitric oxide (NO) and other reactive oxygen species (ROS) directly by measurement of chemiluminescence (CL) and to investigate the role of L-arginine, a nitric oxide synthase (NOS) substrate, and N-G-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, together with their molecular enantiomers D-arginine and D-NAME, in a rat mesenteric ischaemia-reperfusion (I/R) model. 2, Seventy-nine female Wistar albino rats were divided into eight groups, The first three groups underwent sham operation; group 1 was the control group, group 2 received L-arginine and group 3 received L-NAME. Ischaemia was produced in the remaining five groups by ligation of the superior mesenteric artery for 30 min followed by 60 min reperfusion, Group 4 rats were control I/R rats and groups 5-8 received either L-arginine, L-NAME, D-arginine or D-NAME, respectively. 3, Both luminol and lucigenin CL was significantly increased in I/R groups compared with sham-operated groups. L-Arginine significantly reduced CL measurements. D-Arginine was also protective, but not as much as L-arginine. Both L- and D-arginine had in vitro O-2(.-)-scavenging potential, as tested by the xanthine-xanthine oxidase system. N-G-Nitro-L-arginine methyl ester decreased lipid peroxidation values in addition to reducing CL measurements. Nitric oxide concentrations were significantly increased in VR groups in comparison with sham-operated groups. Peroxynitrite formation was increased by I/R. Treatment with L-NAME was beneficial by reducing NO concentrations in the reperfused ileum, 4, In our I/R model, O-2(.-), NO and other ROS were increased. Although NOS inhibitors were effective in reducing oxidative damage, increasing NO concentrations with L-arginine was also beneficial, presumably due to the ability of L-arginine to inhibit phagocyte adherence and its radical scavenging potential. In fact, NO may have different effects in terms of tissue injury or protection depending on the concentration of oxygen and the haemodynamic state of the tissue.Publication Metadata only The roles of free oxygen radicals, nitric oxide, and endothelin in caustic injury of rat esophagus(W B SAUNDERS CO-ELSEVIER INC, 2004) DAĞLI, EMRULLAH TOLGA; Ozel, SK; Dagli, TE; Yuksel, M; Kiyan, G; Kotiloglu, EPurpose: The authors aimed to find out the roles of free oxygen radicals, nitric oxide (NO), and endothelin (ET) in caustic injury of rat esophagus. Methods: Forty-five Wistar albino rats were used to form 6 groups. The study groups are summarized as 1, sham (S; n = 7); 2, sham + L-arginine (SA; n 7); 3, sham + L-NAME (SN; n = 7); 4, injury (I; n = 8); 5, injury + L-arginine (IA; n = 8); 6, injury + L-NAME (IN; n = 8). Normal saline in the sham groups and 50% NaOH in the caustic injury groups were administered to the distal esophagus. Free oxygen radicals and NO were detected by chemiluminescence from tissue samples, and they were correlated with histologic examinations. Tissue ET was measured also with immunohistochemistry. Results: The injury was verified histologically. Free oxygen radical levels were found to be increased as well as NO and ET with the caustic injury (P < .05). L-arginine caused a histologic increase in the injury that was close to statistical significance (P = .08). L-NAME showed no significant effect. Conclusions: Free radicals, NO, and ET increase in the early phase of caustic esophageal injury. Understanding their early interactions during the caustic injury may help in future therapeutic strategies. (C) 2004 Elsevier Inc. All rights reserved.Publication Metadata only Nitric oxide and endothelin relationship in intestinal ischemia/reperfusion injury (II)(CHURCHILL LIVINGSTONE, 2001) DAĞLI, EMRULLAH TOLGA; Ozel, SK; Yuksel, M; Haklar, G; Durakbasa, CU; Dagli, TE; Aktan, AOEndothelins (ETs) are potent vasoconstrictors derived from vascular endothelium. They have primary roles in many pathophysiologic states including ischemia/reperfusion (I/R) injury. The relationships between nitric oxide (NO) and ETs are still under investigation. In this study on rats we want to focus on the interaction of NO and ET especially in I/R injury. For this purpose ET-1 and PD-156252, a nonselective ET receptor blocker, were given in a mesenteric I/R model and reactive oxygen species were detected directly using chemiluminescence of the ileal tissue. ET administrations to sham and I/R groups caused significant increases in NO concentrations whereas, in terms of peroxynitrite, which is a highly reactive group of free radicals, its increasing effects were seen only in I/R groups. This suggests that in I/R where superoxide levels increase together with NO, the conversion to peroxynitrite is likely and this effect is augmented with ET administration. On the other hand PD administration decreases superoxide and thereby peroxynitrite levels and this study shows that the effect of PD-156252 is established through this mode of action. These data suggest therapeutic approaches that may be beneficial in the treatment of I/R injury. (C) 2001 Harcourt Publishers Ltd.Publication Metadata only Nitric oxide and endothelin relationship in intestinal ischemia/reperfusion injury(1998) DAĞLI, EMRULLAH TOLGA; Durakbasa, C. U.; Dagli, T. E.; Mouni, H.; Haklar, G.; Bilsel, A. S.; Yuksel, M.; Aktan, A. O.Gastrointestinal mucosal blood flow is dependent on a balanced release of vasoactive substances from endothelium. Nitric oxide (NO) may increase the flow by vasodilatation and/or antiaggregation whereas endothelin (ET) may decrease it by vasoconstriction and aggregation. NO and ET may have counterbalancing effects on each other in tissue damage. In order to test this hypothesis, in this study on rats, L-arginine to increase NO levels and N(G)-nitro-L-arginine methyl esther (L-NAME) to decrease NO levels have been used in an intestinal ischemia/ reperfusion (I/R) injury model and portal vein ET response was evaluated. Lipid peroxidation product measurements and chemiluminescence (CL) studies were also carried out in ileal tissue samples. Intestinal I/R injury caused an increase in portal venous ET levels with levels of 9.4+/-0.5 fmol/ml in sham operation and 14.8+/-1.6 fmol/ml in I/R group. ET level of L-NAME-sh group was lower than that of sham-operated group and also ET level of L-NAME-I/R group was lower than that of I/R group. This yielded the conclusion that inhibition of NO synthesis decreases portal venous ET levels in this model. Increased NO production by L-arginine caused increased ET levels in sham operated groups but this effect was not observed in I/R injury state. This study also showed that inhibition of NO synthesis has a protective role by reducing the reperfusion damage in this model. It is likely that NO and ET have a feedback effect on each other both under physiologic conditions and I/R injury.