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    Brain tissue biochemical parameters in cerebral ischemic reperfusion injury after hemorrhagic shock: An experimental study
    (UNIVERSITATSVERLAG ULM GMBH, 2007) Cosar, Murat; Eser, Olcay; Fidan, Hueseyin; Kalkan, Erdal; Buyukbas, Sadik; Ozen, O. A.
    Objective: In this study, we showed the tissue biochemical parameters in cerebral ischemic reperfusion injury that developed after hemorrhagic shock in a rat model. Materials and Methods: Hemorrhagic shock models were established in 36 adult Sprague-Dawley rats and divided into six groups: control (group A), hemorrhagic shock (HS) (group B), first hour ischemic reperfusion (IR+1h) (group Q, 311 hour IR (IR+3h) (group D), 61(th) hour IR (IR+6h) (group E) and 2411 hour IR (IR+24h) (group F). The rats were sacrificed by bleeding from the intracardiac area after finishing the experiment. The brains were removed from the skull immediately. Bilateral hemispheres were dissected for biochemical analyses, and activities of superoxide dismutase (SOD) and myeloperoxidase (MPO), and the levels of malondialdehyde (MDA) were evaluated. Results: The study revealed that the SOD activities decreased stepwise from group A (control) to group F (IR+24h) (P<0.05). In addition, MDA levels and MPO activities increased stepwise from group A (control) to group F (IR+24h). Conclusion: We think that the level of cell injury increases stepwise in the first, 3(rd), 6(th) and 24(th) hours after ischemia reperfusion injury.
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    The evaluation of protective effects of FK-506 on neural ischemic-reperfusion injury: an experimental study
    (SPRINGER HEIDELBERG, 2007) Eser, Olcay; Kalkan, Erdal; Cosar, Murat; Yaman, Mehmet; Buyukbas, Sadik; Avunduk, Mustafa Cihat; Fidan, Hueseyin
    Objective: In this study, we aimed to delineate the mode of neuroprotective action of FK-506, and demonstrated that FK-506 could decrease oxidative stress and apoptotic cell death in an in vivo rat model of neural ischemia-reperfusion after hemorrhagic shock. Methods: Thirty rats were used as experimental subjects and divided into five equal groups. Group A rats (sham group, n = 6) were anesthetized and craniotomies were performed for collecting brain tissue samples. In group B ischemia-reperfusion (I/R + 1 h, n = 6), group C (I/R + 24 h, n = 6), group D (I/R + 1 h FK-506, n = 6) and group E (I/R + 24 h FK-506, n = 6), systolic blood pressure of the rats decreased to 40-50% of the normal level via bleeding from the femoral vein. Thus, a hemorrhagic shock and ischemic neural tissue model was formed. The blood was retained and given to the remaining animals in groups B, C, D and E via femoral vein for reperfusion 20 min after the procedure. In group D and E, 1 mg/kg FK-506 in 0.5 ml isotonic solution was administered to the rats 5 min before reperfusion. Group B and D rats were sacrificed after 1 hand group C and E rats were sacrificed 24 h after reperfusion; the rats were sacrificed via bleeding associated with intracardiac puncture. Craniotomy was also performed in groups B, C, D and E and brain tissue samples were fixed using neutral buffered 10% formaldehyde solution for immunohistopathological examination as in group A. Brain tissue superoxide dismutase (SOD) activities, malondialdehyde (MDA) levels, tissue myeloperoxydase (MPO) activities and apoptotic cell analyses with APO 2.7 immunohistochemically were also performed in all groups. Results: The result of the study revealed that the SOD activities were lower for groups B (I/R + 1 h) and C (I/ R + 24 h) than for group A (sham group) (p < 0.05). In addition, SOD activities were higher in groups D (I/ R + 1 h FK-506) and E (I/R + 24 h FK-506) than in groups B (I/R + 1 h) and C (I/R + 24 h) (p < 0.05). MDA levels, MPO activities and the number of apoptotic cells were lower in group A (sham group) than in groups B (I/R + 1 h) and C (I/R + 24 h) (p < 0.05). In addition to these MDA levels, MPO activities and the number of apoptotic cells were higher in groups B (I/R + 1 h) and C (I/R + 24 h) as compared to groups D (I/R + 1 h FK-506) and E (I/R + 24 h FK-506) (p < 0.05). Conclusion: The results suggest that the prophylactic use of FK-506 in an in situ ischemic neural tissue may prevent reperfusion injury.