Literature DB >> 10455917

Macrophage depletion alters vein graft intimal hyperplasia.

J R Hoch1, V K Stark, N van Rooijen, J L Kim, M P Nutt, T F Warner.   

Abstract

BACKGROUND: The principal cause of vein graft failure is intimal hyperplasia (IH); however, its etiology remains unclear. In a rat model of vein graft IH we have observed prolonged transmural macrophage infiltration, leading us to hypothesize that these cells regulate IH. To test this, we used liposome-encapsulated dichloromethylene bisphosphonate (L-Cl2MBP) to deplete rat macrophages and observed the effects on IH.
METHODS: Epigastric vein-to-femoral artery grafts were microsurgically placed in male Lewis rats that had been intravenously injected with L-Cl2MBP, phosphate-buffered saline solution liposomes, or phosphate-buffered saline solution alone 2 days before surgery. Several animals in each group received a second equivalent dose at 2 weeks. Grafts, contralateral epigastric veins, spleens, and livers were harvested at 1, 2, and 4 weeks for histologic examination, immunohistochemistry, and transmission electron microscopy.
RESULTS: In the L-Cl2MBP-treated animals splenic and hepatic macrophages were greatly reduced, confirming the efficacy of the agent. At 1 to 2 weeks graft macrophages were significantly decreased, and there was a trend toward decreased IH. At 4 weeks macrophage numbers were normal and IH development had resumed. In contrast, the 4-week grafts treated with 2 doses of L-Cl2MBP had fewer macrophages and displayed severely attenuated IH.
CONCLUSIONS: The results indicate a suppression of IH as macrophages are depleted, with a resumption of the process as macrophages repopulate the graft.

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Year:  1999        PMID: 10455917

Source DB:  PubMed          Journal:  Surgery        ISSN: 0039-6060            Impact factor:   3.982


  23 in total

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