Person: YALÇIN, AHMET SUHA
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YALÇIN
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AHMET SUHA
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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 Effects of N-acetylcysteine on myocardial ischemia-reperfusion injury in bypass surgery(SPRINGER, 2006) YALÇIN, AHMET SUHA; Orhan, G; Yapici, N; Yuksel, M; Sargin, M; Senay, S; Yalcin, AS; Aykac, Z; Aka, SAMyocardial ischemia-reperfusion injury may complicate coronary artery bypass grafting (CABG) operations. N-Acertylcysteine (NAC) had antioxidant and microcirculatory effects, and inhibits neutrophil aggregation. The aim of this study was to determine the effects of NAC in limiting myocardial ischemia-reperfusion injury in CABG operations. Twenty patients undergoing elective coronary bypass operation with cardiopulmonary bypass were enrolled and randomly assigned to two groups: a control group operated with a routine CABG protocol, and one where NAC was administered intravenously during the operation (NAC group). Blood samples from coronary sinus for tumor necrosis factor-alpha assay, myocardial biopsy specimens for chemiluminescent luminol, and lucigenin measurements of reactive oxygen species were taken. The luminol (specific for .-OH, H2O2, and HOCl- radicals) and lucigenin (specific for O-2(.-)) levels and the difference ratios after reperfusion were significantly lower in the NAC group. Tumor necrosis factor-alpha levels increased in the control group but, in contrast, a significant decrease was detected in the NAC group (P < 0.01). Creatine kinase-MB levels at 6 and 12 hours were singnificantly lower in the NAC group (P = 0.02). N-Acetylcysteine has potential effects to limit ischemia reperfusion injury during CABG operations. We believe that its effects on clinical outcome may be more apparent in patients prone to ischemia-reperfusion injury.