Relationship of TGF-beta1 mRNA Expression and Captopril after PTFE Graft in Rabbit Carotid Artery.
- Author:
Jun Won UM
1
;
Young Sik KIM
;
Suk In JUNG
;
Sang Yong CHOI
;
Cheung Wung WHANG
Author Information
1. Department of General Surgery, Korea University College of Medicine, Seoul, Korea. cwwhang@unitel.co.kr
- Publication Type:Original Article
- Keywords:
Intimal hyperplasia;
TGF-beta 1;
PTFE;
Angiotensin-converting enzyme inhibitor;
Rabbits
- MeSH:
Angiotensin II;
Captopril*;
Carotid Arteries*;
Cell Proliferation;
Hyperplasia;
Muscle, Smooth, Vascular;
Myocytes, Smooth Muscle;
Polytetrafluoroethylene*;
Rabbits;
Renin-Angiotensin System;
RNA, Messenger*;
Transforming Growth Factor beta1*;
Transplants*
- From:Journal of the Korean Society for Vascular Surgery
1999;15(2):195-204
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Intimal hyperplasia (IH) due to vascular smooth muscle cell proliferation is a leading cause of late vascular graft failure. Transforming growth factor-beta1 (TGF-beta1), 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-beta1 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-beta1 mRNA expression, and effect of angiotensin-converting enzyme inhibitor (ACEI) 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 ACEI). 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 grafts. Intimal hyperplasia was defined by the intima to media height ratio (IMHR). The mRNA expression of TGF-beta1 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-beta1 in graft with ACEI was lower than that in graft only (p<0.05). In summary, there was evidence that TGF-beta1 is closely related with intimal hyperplasia and there is also relationship between ANG II and TGF-beta1. CONCLUSION: ANG II and TGF-beta1 may mediate intimal hyperplasia of vascular graft, and ACE inhibitor may be a armamentarium for inhibition of intimal hyperplasia in vascular graft procedures.
