Journal Title
Title of Journal: Cardiovasc Drugs Ther
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Abbravation: Cardiovascular Drugs and Therapy
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Authors: Michael Hack Frank G Mascha Bertram J Jobst Guenter A J Riegger Daniel P Griese
Publish Date: 2008/06/05
Volume: 22, Issue: 5, Pages: 351-362
Abstract
Percutaneous vascular interventions lead inevitably to a destruction of the endothelial lining at the site of injury There are conflicting data on the therapeutic benefit of hematopoietic growth factors aiming at mobilisation of circulating endothelial cells to accelerate the reendothelialisation process Aim of our study was to evaluate the impact of a maximised 7 daycombination therapy with GCSF plus EPO on the healing process following balloon injury of the rat carotid arteryOsmotic pumps to systemically deliver GCSF and EPO at saturating doses during the first seven days post injury were implanted into the peritoneal cavity of splenectomised male Sprague–Dawley rats Cytokine treatment resulted in significantly elevated numbers of white blood cells hematocrit levels circulating hematopoietic stem cells and—temporarily—circulating endothelial precursors Functional reendothelialisation as assessed by Evan’s blue staining on day 14 post injury was not affected by the cytokine treatment The neointimal response was analysed on day 7 and 28 post injury and was significantly higher at the day 7 timepoint Cytokines I/Mratio 110 ± 009 vs Saline 036 ± 006 Cytokine treated rats also displayed higher rates of thrombotic occlusion Cytokines 25–33 vs Saline 0 Serum levels of PAI1 TGFβ1 and PDGFBB were not elevated in the cytokine treated rats The proliferative rates both in the injured vessel wall and the surrounding adventitia as assessed by BrdU incorporation were significantly higher in the cytokine treated animals The number of CD45pos hematopoietic cells was significantly higher in the adventitia of the cytokine treated rats Vasa vasorum were not found to be significantly different The increased neointimal response was not due to expression of GCSF or EPOreceptors on VSMCs within the vessel wall or myofibroblasts in the adventitia
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