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dc.contributor.authorYucel, Semih
dc.contributor.authorBahcivan, Muzaffer
dc.contributor.authorGol, Mehmet Kamil
dc.contributor.authorErenler, Behice H.
dc.contributor.authorKolbakir, Fersat
dc.contributor.authorKeceligil, Hasan T.
dc.date.accessioned2020-06-21T14:54:35Z
dc.date.available2020-06-21T14:54:35Z
dc.date.issued2009
dc.identifier.issn1526-6702
dc.identifier.urihttps://hdl.handle.net/20.500.12712/18434
dc.descriptionKECELIGIL, HASAN TAHSIN/0000-0002-8256-8059en_US
dc.descriptionWOS: 000270688600006en_US
dc.descriptionPubMed: 19876413en_US
dc.description.abstractIntimal hyperplasia is a major cause of restenosis after the interventional or surgical treatment of occlusive arterial disease. We investigated the effects of clopidogrel, calcium dobesilate, nebivolol, and atorvastatin on the development of intimal hyperplasia in rabbits after carotid venous bypass surgery We divided 40 male New Zealand rabbits into 4 study groups and I control group. After occluding the carotid arteries of the rabbits, we constructed jugular venous grafts between the proximal and the distal segments of the occluded artery Thereafter, group I (control) received no medication. We administered daily oral doses of clopidogrel to group 2, calcium dobesilate to group 3, nebivolol to group 4, and atorvastatin to group 5. The rabbits were killed 28 days postoperatively The arterialized jugular venous grafts were extracted for histopathologic examination. Intimal thicknesses were 42.87 +/- 6.95 mu m (group 2), 46.5 +/- 9.02 mu m (group 3), 34.12 +/- 5.64 mu m (group 4), and 48.37 +/- 6.16 mu m (group 5), all significantly less than the 95.12 +/- 9.93 mu m in group 1 (all P <0.001). Medial thicknesses were 94 +/- 6 mu m (group 2), 107.5 +/- 13.52 mu m (group 3), 90.5 +/- 9.69 mu m (group 4), and 101.37 +/- 7.99 mu m (group 5), all significantly thinner than the 126.62 +/- 13.53 mu m in group 1 (all P <0.001). In our experimental model of carotid venous bypass grafting in rabbits, clopidogrel, calcium dobesilate, nebivolol, and atorvastatin each effectively reduced the development of intimal hyperplasia. Herein, we discuss our findings and review the medical literature. (Tex Heart Inst J 2009,36(5):387-92)en_US
dc.language.isoengen_US
dc.publisherTexas Heart Insten_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAnastomosis, surgicalen_US
dc.subjectcardiovascular agents/administration & dosageen_US
dc.subjectcarotid arteries/drug/effects/pathology/surgeryen_US
dc.subjectcarotid stenosis/prevention & controlen_US
dc.subjectcoronary artery disease/drug therapy/prevention & controlen_US
dc.subjectcoronary restenosis/drug therapyen_US
dc.subjectdisease models, animalen_US
dc.subjecthyperplasia/drug therapy/etiology/prevention & controlen_US
dc.subjectjugular veins/transplantationen_US
dc.subjectrabbitsen_US
dc.subjecttunica intima/drug effects/pathologyen_US
dc.titleReduced Intimal Hyperplasia in Rabbits via Medical Therapy after Carotid Venous Bypassen_US
dc.typearticleen_US
dc.contributor.departmentOMÜen_US
dc.identifier.volume36en_US
dc.identifier.issue5en_US
dc.identifier.startpage387en_US
dc.identifier.endpage392en_US
dc.relation.journalTexas Heart Institute Journalen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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