Yazar "Alpay, Mehmet Fatih" seçeneğine göre listele

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    A fatal complication after repair of post-infarction ventricular septal rupture: heparin-induced thrombocytopenia with thrombosis
    (Clinics Cardive Publ Pty Ltd, 2015) Nazli, Yunus; Colak, Necmettin; Demircelik, Bora; Alpay, Mehmet Fatih; Cakir, Omer; Cagli, Kerim
    Heparin-induced thrombocytopenia (HIT) is a rare but potentially devastating and life-threatening complication from using heparin. HIT not only causes thrombocytopenia, but it also carries an increased risk for fatal thrombotic complications. In this report, we describe the case of a patient in whom fatal HIT developed after successful surgical repair of a posterior post-infarction ventricular septal rupture with cardiopulmonary bypass.
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    Assessment of the efficacy of Ankaferd blood stopper on the prevention of postoperative pericardial adhesions
    (Clinics Cardive Publ Pty Ltd, 2014) Nazli, Yunus; Colak, Necmettin; Alpay, Mehmet Fatih; Haltas, Hacer; Aksoy, Omer Nuri; Akkaya, Ismail Olgun; Cakir, Omer
    Objectives: Ankaferd has been used as a blood-stopping agent and it may also have an anti-inflammatory effect. We investigated the efficacy of Ankaferd in preventing postoperative pericardial adhesions in an experimental rabbit model. Methods: Sixteen New Zealand white rabbits were used and categorised into two groups: an Ankaferd and a control group. The Ankaferd group of rabbits was treated with a sponge impregnated with Ankaferd solution, which was applied over the abraded epicardium. A sponge impregnated with 0.9% isotonic NaCl solution was applied to the control group using the same protocol. Scores for adhesion and visibility of coronary vessels were graded by macroscopic examination, and pericardial tissues were analysed microscopically in terms of inflammation and fibrosis. Results: In the Ankaferd group, the adhesion scores were significantly higher than in the control group (p = 0.007). When the groups were compared according to the prevalence of fibrosis and degree of inflammation, the Ankaferd group was found to be statistically significantly different from the control group in terms of prevalence of fibrosis (p = 0.028). Conclusion: Topical application of Ankaferd to prevent postoperative pericardial adhesions increased adhesion and fibrosis scores.
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    Cilostazol Attenuates Spinal Cord Ischemia-Reperfusion Injury in Rabbits
    (W B Saunders Co-Elsevier Inc, 2015) Nazli, Yunus; Colak, Necmettin; Namuslu, Mehmet; Erdannar, Husamettin; Haltas, Hacer; Alpay, Mehmet Fatih; Aksoy, Omer Nuri
    Objective: The aim of this study was to evaluate the pretreatment effect of cilostazol on spinal cord ischemia-reperfusion injury. Design: Prospective, interventional study. Setting: Research laboratory, single institution. Participants: Twenty-four New Zealand white rabbits. Interventions: Twenty-four rabbits were divided into 3 equal groups: group I (sham), group II (ischemia-reperfusion, control group), and group III (cilostazol, administered orally 30 mg/kg/day for 3 days before the surgery). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the iliac bifurcation for 30 minutes. Seventy-two hours postoperatively, the motor function of the lower limbs was evaluated in each animal according to the modified Tarlov score. Spinal cord and blood samples were taken for histopathologic and biochemical analyses at the 72nd hour of reperfusion. Measurements and Main Results: All rabbits in the ischemia-reperfusion group (group II) showed severe neurologic deficits. The median (IQR) Tarlov scores postoperatively at 72 hours in groups I, II, and III were 5.0(-), 2.0(1.0), and 4.5(1.0), respectively. Administration of cilostazol resulted in a significant reduction in motor dysfunction when compared with the ischemia-reperfusion group (p < 0.001). In the ischemia-reperfusion group, serum and tissue glutathione peroxidase and superoxide dismutase activity were significantly less compared with the sham group (group I) (p < 0.05). Serum and tissue glutathione peroxidase and superoxide dismutase levels in the cilostazol-treated group (group III) were higher compared with the ischemia-reperfusion group (p < 0.05). In the cilostazoltreated group, serum and tissue malondialdehyde levels were lower compared with the ischemia-reperfusion group (p < 0.05). Histopathologic analysis found decreased neuronal injury in the cilostazol group when compared with the ischemia-reperfusion group (p < 0.05). Conclusions: This study showed that pretreatment with cilostazol significantly ameliorated neurologic functional outcome and attenuated neuronal histopathologic injury after transient aortic occlusion in rabbits. (C) 2015 Elsevier Inc. All rights reserved.
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    Neuroprotective effect of atorvastatin in spinal cord ischemia-reperfusion injury
    (Hospital Clinicas, Univ Sao Paulo, 2015) Nazli, Yunus; Colak, Necmettin; Alpay, Mehmet Fatih; Uysal, Sema; Uzunlar, Ali Kemal; Cakir, Omer
    OBJECTIVES: Prevention of the development of paraplegia during the repair of the damage caused by descending thoracic and thoracoabdominal aneurysms remains an important issue. Therefore, we investigated the protective effect of atorvastatin on ischemia-induced spinal cord injury in a rabbit model. METHOD: Thirty-two rabbits were divided into the following four equally sized groups: group I (control), group II (ischemia-reperfusion), group III (atorvastatin treatment) and group IV (atorvastatin withdrawal). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the iliac bifurcation. Seventy-two hours postoperatively, the motor function of the lower limbs of each animal was evaluated according to the Tarlov score. Spinal cord and blood samples were obtained for histopathological and biochemical analyses. RESULTS: All of the rabbits in group II exhibited severe neurological deficits. Atorvastatin treatment (groups III and IV) significantly reduced the level of motor dysfunction. No significant differences were observed between the motor function scores of groups III and IV at the evaluated time points. Light microscopic examination of spinal cord tissue samples obtained at the 72nd hour of reperfusion indicated greater tissue preservation in groups III and IV than in group II. CONCLUSION: This study demonstrates the considerable neuroprotective effect of atorvastatin on the neurological, biochemical and histopathological status of rabbits with ischemia-induced spinal cord injury. Moreover, the acute withdrawal of atorvastatin therapy following the induction of spinal cord ischemia did not increase the neuronal damage in this rabbit model.