Tumor necrosis factor-α expression in rat models of intimal hyperplasia

Mitsuhiro Yamamura; Takashi Miyamoto; John R. Hoch

doi:10.1007/BF01616406

International Journal of Angiology, Table of Contents

Int J Angiol 2001; 10(2): 77-79
DOI: 10.1007/BF01616406

Original Articles

Tumor necrosis factor-α expression in rat models of intimal hyperplasia

Mitsuhiro Yamamura¹ , Takashi Miyamoto¹ , John R. Hoch²

¹Department of Cardiovascular Surgery, Hyogo College of Medicine, Hyogo, Japan
²Department of Surgery, University of Wisconsin-Madison, Wisconsin

This work was performed at the Dept. of Surgery, University of Wisconsin-Madison, U.S.A. and was presented in part as the recipient of the Professor Albert Senn Young Investigator Award during the 42nd Annual World Congress, International College of Angiology, San Diego, California, June 2000.

Abstract

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Abstract

Today most cardiovascular surgeons prefer artery grafts to vein grafts, because of their better long term patency. Recently we reported monocyte/macrophage infiltration and the development of intimal hyperplasia (IH) is different in rat epigastric vein to common femoral artery interposition graft, from common femoral artery transection and re-anastomosis. Tumor Necrosis Factor-α (TNF-α) has been well known as one of the growth factors produced from activated macrophages. We hypothesize TNF-α mRNA expression is different in vein graft compared to femoral artery re-anastomosis. Lewis rats underwent either epigastric vein to common femoral artery interposition grafts (VG: n=25) or common femoral artery transection and re-anastomoses (FA: n=24). Vessels were harvested at 0 hour, 1 hour, 3 hours, 1 day, 4 days, 1 week and 2 weeks. To compare the development of IH, vessel wall areas were calculated and described as the intimal area/total area (Ri). TNF-α mRNA expression was examined by using reverse transcription-polymerase chain reaction, and was compared with S-26 mRNA expression on computerized densitometry. The TNF-α/S-26 mRNA expression ratio was increased in VG compared to FA re-anastomosis, especially at 1 week (p<0.01). These results suggest that the mechanism of IH is different between vein graft and artery graft. Japanese patients [1–4]. The majority of bypass failures occur within the first two years, due to the process of intimal hyperplasia (IH) which begins as early as one month after operation [5]. Recently we reported monocyte/macrophage infiltration, and the development of IH is different in rat epigastric vein to common femoral artery interposition graft (VG), from common femoral artery transection & reanastomosis (FA) [6]. Tumor Necrosis Factor-α (TNF-α) has been well known as one of the growth factors produced from activated macrophages [7]. To study the mechanism of IH, we hypothesize TNF-α mRNA expression is different in VG from FA re-anastomosis.

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