Basic & Clinical Medicine ›› 2011, Vol. 31 ›› Issue (11): 1267-1272.

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Ex vivo activated macrophages myocardial transplantation improve the ventricular remodeling of the infarcted heart induced by ischemia/reperfusion

He LI   

  • Received:2011-05-04 Revised:2011-07-07 Online:2011-11-05 Published:2011-11-02
  • Contact: He LI

Abstract: Objective To investigate the mechanism of the paracrine effect of phenytoin (PHT) and macrophage in the angiogenesis and ventricular remodeling after myocardial infarction (MI). Method The peritoneal macrophages were adherently cultured, and parts of cultured macrophages were pre-stimulated by PHT. The survival animals induced experimental ischemia-reperfusion (I/R) were randomly distributed into Sham group, control (AMI) group, Phenytoin (PHT) group group, macrophage (MΦ) group, phenytoin pre-stimulating macrophage (MΦ-PHT) group. At the 7th and 28th day after the induction of I/R, histology examination were analyzed including index of expansion, fiber area, arterioles density, capillary density in infarct region and cardiocyte cross-sectional area (CSA) in non-infarct zone. The levels of protein expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) within infarct region 7 days after MI were determined by Western blot. Result Compared with AMI group, Index of Expansion, fiber area and CSA in non-infarct zone at 28th day were all decreased in PHT group, MΦ group and MΦ-PHT group (P <0.05), while arteriole density in infarct zone had increased (P <0.05). Fiber area of MΦ-PHT group at 28th day was fewer than MΦ group (P <0.05). Compared with MΦ group, capillary density and arteriole density in infarct zone at 7th and 28th day had increasing tendency. The levels of VEGF, bFGF protein expression in infarct zone at 7th day in MΦ-PHT group were more than MΦ group (P <0.05). Conclusion Phenytoin may promote angiogenesis in infarct zone and improve ventricular remodeling after MI through stimulating macrophages, which up-regulate the growth factors involved in the angiogenesis through the paracrine effect.