Answers are grounded in this paper and cite their sources.
The proliferation of intimal smooth muscle cells (SMCs) in large muscular arteries and veins often occurs after surgical interventions such as angioplasty and bypass grafting, and may lead to restenosis and graft failure. Clinical observations suggest that increased pulsatile deformation of veins grated into an arterial position may play a role in intimal hyperplasia. Since intimal hyperplasia occurs at the vein/arterial interface of the graft, SMC hyperplasia could be due to the proliferation of either aortic or venous SMCs. Therefore, we compared the effects of in vitro mechanical deformation on the proliferation of aortic SMCs with venous SMCs. Using the Flexercell apparatus (Flexercell Corp., McKeesport, Pa., USA), aortic SMCs, stretched at 3 and 60 cpm did not lead to a significant increase in growth as compared to the nonstretched controls. In contrast, stretch of venous SMCs at 3 and 60 cpm led to a significant increase in growth as compared to the nonstretched controls. These results suggest that the SMC proliferation, as occurs in vein interposition grafts in vivo, may be partially due to a stimulatory response by venous SMCs to increased mechanical stimulation.
No takes yet. Share an insight, caveat, or question.
Dethlefsen et al. (2008) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: