S Yazici1, S Demirtas2, O Guclu2, O Karahan2, C Yavuz2, A Caliskan2, B Mavitas2. 1. Department of Cardiovascular Surgery, Medical School of Dicle University, Diyarbakir, Turkey yazici.suleyman@hotmail.com. 2. Department of Cardiovascular Surgery, Medical School of Dicle University, Diyarbakir, Turkey.
Abstract
OBJECTIVE: The aim of this study was to determine the relationship between oxidative stress markers and the duration of ischemia in rat mesenteric and peripheral ischemia models. METHODS: Forty rats were divided into five equal groups, as follows: rats in Group I (control group) were sacrificed to determine the baseline characteristics of the serum markers; the superior mesenteric artery was clamped via a simple laparotomy to induce mesenteric ischemia in Groups II and III; the right common femoral artery was clamped to induce peripheral ischemia in Groups IV and V. Blood samples were taken at 2 (Groups II and IV) and 6 (Groups III and V) hours after these procedures. The serum total oxidative status (TOS), total antioxidant capacity (TAC), oxidative stress index (OSI) and paraoxonase-1 (PON-1) enzyme activities were evaluated in the samples obtained from each group. RESULTS: The OSI level of the control group was 91.00±5.46 (mean ± SD). The OSI levels taken 2 hours after the induction of mesenteric ischemia and peripheral ischemia were significantly higher (194.50±11.16 and 301.75±19.98, respectively (p<0.05)). However, these levels decreased to 151.88±17.02 (mesenteric ischemia) and 108.88±9.46 (peripheral ischemia) after 6 hours. The PON-1 levels of Group III (mesenteric ischemia at 6 hours) (99.75±7.26), Group IV (peripheral ischemia at 2 hours) (96.88±4.09), and Group V (peripheral ischemia at 6 hours) (111.25±10.33) were slightly elevated over that of the control group (87.38±5.31). However, the PON-1 level of Group II (mesenteric ischemia at 2 hours) (42.88±3.14) was lower than that of the other groups (p<0.05). CONCLUSION: Despite the increment of oxidative markers in early periods of ischemia (2(nd) hour), which was a hypoxic response of ischemic cells, they have decreased markedly in prolonged ischemia. This might have been caused by the opening of some collateral circulation or the destruction of the ischemic cells.
OBJECTIVE: The aim of this study was to determine the relationship between oxidative stress markers and the duration of ischemia in rat mesenteric and peripheral ischemia models. METHODS: Forty rats were divided into five equal groups, as follows: rats in Group I (control group) were sacrificed to determine the baseline characteristics of the serum markers; the superior mesenteric artery was clamped via a simple laparotomy to induce mesenteric ischemia in Groups II and III; the right common femoral artery was clamped to induce peripheral ischemia in Groups IV and V. Blood samples were taken at 2 (Groups II and IV) and 6 (Groups III and V) hours after these procedures. The serum total oxidative status (TOS), total antioxidant capacity (TAC), oxidative stress index (OSI) and paraoxonase-1 (PON-1) enzyme activities were evaluated in the samples obtained from each group. RESULTS: The OSI level of the control group was 91.00±5.46 (mean ± SD). The OSI levels taken 2 hours after the induction of mesenteric ischemia and peripheral ischemia were significantly higher (194.50±11.16 and 301.75±19.98, respectively (p<0.05)). However, these levels decreased to 151.88±17.02 (mesenteric ischemia) and 108.88±9.46 (peripheral ischemia) after 6 hours. The PON-1 levels of Group III (mesenteric ischemia at 6 hours) (99.75±7.26), Group IV (peripheral ischemia at 2 hours) (96.88±4.09), and Group V (peripheral ischemia at 6 hours) (111.25±10.33) were slightly elevated over that of the control group (87.38±5.31). However, the PON-1 level of Group II (mesenteric ischemia at 2 hours) (42.88±3.14) was lower than that of the other groups (p<0.05). CONCLUSION: Despite the increment of oxidative markers in early periods of ischemia (2(nd) hour), which was a hypoxic response of ischemic cells, they have decreased markedly in prolonged ischemia. This might have been caused by the opening of some collateral circulation or the destruction of the ischemic cells.
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