가토의 경동맥 PTEE 이식 후 변형 성장인자 발현과 ACE Inhibitor 투여에 따른 변화

Purpose: Intimal hyperplasia (IH) due to vascular smooth muscle cell proliferation is a leading cause of late vascular graft failure. Transforming growth factor-β1 (TGF-β1), known to influence smooth muscle cell growth in vascular wall has been subjected for experimental research as a cause of IH. It has been also showed that IH can be mediated by local renin-angiotensin system in vascular intimal injury. Under the assumption that TGF- β1 and local angiotensin II (ANG II) have a major role as a cause of IH, we carried out this study to see if there are any relationship between intimal hyperplasia and TGF- β1 mRNA expression, and effect of angiotensinnverting enzyme inhibitor (ACE#p on IH. Methods: 14 New Zealand White rabbits were subjected for this experiment. The right carotid arteries of 14 rabbits had been bypass grafting with polytetrafluoroethylene. 14 rabbits were allocated into two groups: 7 rabbits had bypass grafting only (graft only) and the other 7 rabbits had bypass grafting with ACEI (graft with ACE1). The rabbits, graft with ACEI were on Captopril (10 mg/kg/day PO) from day of operation to 8 weeks when to harvest. There were patent 9 carotid bypass grafts at harvest, and the studies were performed in patent .Intimal hyperplasia was defined by the intima to media height ratio (IMHR). The mRNA expression of TGF-β1 was determined by semiquantitative RT-PCR. Results: IMHR of graft with ACEI was lower than that of graft (p<0.05). The mRNA expression of TGF-β1 in graft with ACEI was lower than that in graft only (p<0.05). In summary, there was evidence that TGF-β1 is closely related with intimal hyperplasia and there is also relationeship between ANG II and TGF-β1. Conclusion: ANG II and TGF-β1 may mediate intimal hyperplasia of vascular graft, and ACE inhibitor may be a armamentarium for inhibition of intimal hyperplasia in vascular graft procedures.