Abstract Microsurgical models of vein-to-artery graft surgery have been developed in rats as a means of as- sessing vein graft adaptation and neo-intimal hyperpla- sia. Neo-intimal hyperplasia in these grafts is often at- tributed, at least in part, to an adaptive response by ve- nous smooth muscle cells to the increased intraluminal pressure of the arterial pressure. However, considerable evidence suggests complete or near-complete cellular re- placement in these grafts. A series of experiments were undertaken in which male vein or artery grafts were placed into either allogeneic female nude rat hosts or in- to syngeneic WKy female hosts as a means of determin- ing donor cell survival. Grafts were removed at postsur- gery week 2 or week 6 and the fate of the donor male cells assessed by PCR amplification of the testis-deter- mining gene Sry. The Sry gene was undetectable in 2-week male to female vein grafts. When left for 6 weeks, donor cells were detectable in vein grafts only after multiple 50-cycle PCR analyses. Minimal donor cell survival was not due to an allograft response, as do- nor male cells were readily detectable in WKy male to female nude rat artery-to-artery grafts. These data were not nude rat specific, as poor donor cell survival was also evidenced in syngeneic male to female vein-to-ar- tery grafts. In conclusion, we demonstrate only marginal survival of donor cells in rat vein-to-artery grafts. Neo- intimal hyperplasia in these grafts was not a consequence of donor venous smooth muscle cell proliferation. Keywords Spontaneously hypertensive rat (SHR) · Sry · Artery grafts · WKy · Nude rat Introduction Coronary artery bypass graft (CABG) surgery is fre- quently used to bypass stenoses and occlusions in the coronary arteries. Despite the more frequent use of arte- rial conduit material, the saphenous vein is still the most commonly used donor vessel for this surgery. Vein grafts undergo morphological change as a result of insertion in- to an artery. The vein graft wall thickens largely as a re- sult of neo-intimal hyperplasia. This is a chronic re- sponse that is characterised by smooth muscle cell (SMC) proliferation and infiltration into the tunica inti- ma of the vein segment. The thickened structure is known as a neo-intima and is composed of SMC and ex- tracellular matrix. The neo-intima is similar structurally and functionally to the media of the host artery. It has been proposed that this allows the vein graft to accom- modate the increased intraluminal pressure of the arterial circulation. However, in many cases excessive neo-inti- mal hyperplasia (NIH) contributes to graft failure (Kockx 1995) and may provide a foundation for graft stenosis and atherosclerosis (Schwartz et al. 1995). The causes of vein graft NIH are many. Surgical trau- ma such as anoxia, clamp trauma and suture trauma are all known to contribute to vascular injury and NIH (Redwood et al. 1999). Postsurgical effects such as me- chanical deformations and alterations to flow velocity and shear stress also affect the extent of NIH (Dobrin 1997). Inflammatory responses also play an important role in postsurgical trauma and NIH (Hancock et al. 1994; Hoch et al. 1999). In a rat model of vein-to-artery graft adaptation, inflammatory responses were consider- able, with up to 100% of the cells in day-2 grafts being Mac-1 + monocyte/macrophages and granulocytes (A.J. Redwood, A. Ahmat, and M. Tennant, unpublished work). In human saphenous vein grafts, inflammatory re- sponses are also considerable, with extensive polymor- The authors are most grateful to the Raine Foundation for Medical Research for financial support A.J. Redwood ( ✉ ) · M. Tennant School of Oral Health Sciences, The University of Western Australia, Perth, Nedlands, Western Australia 609, Australia e-mail: aredwood@cyllene.uwa.edu.au Tel.: +61-8-93463587, Fax: +61-8-93462912 Present address: A.J. Redwood, Department of Microbiology, The University of Western Australia, Nedlands, Western Australia 609 Cell Tissue Res (2001) 306:251–256 DOI 10.1007/s004410100435 REGULAR ARTICLE Alec J. Redwood · Marc Tennant Cellular survival in rat vein-to-artery grafts Extensive depletion of donor cells Received: 5 February 2001 / Accepted: 6 February 2001 / Published online: 31 August 2001 © Springer-Verlag 2001