Anastomotic Intimal Hyperplasia and TGF-beta1 mRNA Expression after a PTFE Graft in a Rabbit Carotid Artery

Um, Jun Won; Kim, Young Sik; Jung, Suk In; Choi, Sang Yong; Whang, Cheung Wung

Abstract

BACKGROUND: Intimal hyperplasia 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 the subject of experimental research as a cause of this intimal hyperplasia. Under the assumption that TGF-beta1 has a major role as a cause of intimal hyperplasia, we carried out this study to see if there were any relationship between intimal hyperplasia and TGF-beta1 mRNA expression in vascular bypass graft.
METHODS
21 New Zealand white rabbits were used for this experiment. The right carotid arteries of the 21 rabbits had been bypass grafted with polytetrafluoroethylene (PTFE graft), and the contralateral carotid arteries received sham operations (Control group). The 21 rabbits were allocated into three groups according so that the carotid artery grafts could be harvested at 1, 8, and 14 weeks, respectively. There were 14 patent carotid bypass grafts at harvest (4, 5, and 5 cases according to the postoperative period), and the studies were performed on those 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
The IMHR in the PTFE graft groups increased as time went by from 1 to 14 weeks (p<0.01). The mRNA expressions of TGF-beta1 in PTFE grafts were higher than those in the controls at 1 and 8 weeks (p<0.05). According to sequential changes in the PTFE grafts, the expressions of TGF-beta1 were highest at 8 weeks and lowest at 14 weeks (p<0.05).
CONCLUSIONS
There is evidence that TGF-beta1 is closely related with intimal hyperplasia in vascular bypass graft until 8 weeks after PTFE graft anastomosis.