Preliminary evaluation of a technique for inhibiting intimal hyperplasia: Implantation of a resorbable luminal collagen membrane
Pharmacologic control of intimai hyperplasia has been attempted through oral and intravenous administration of smooth muscle cell inhibitors. We report a more direct method of altering arterial healing using a novel bioresorbable membrane that can be applied to the lumen of an artery or anastomosis following endarterectomy or vascular reconstruction. Following a standard balloon injury, the infrarenal aortas of 3 kg female New Zealand white rabbits were opened and a thin membrane composed of collagen/chondroitin 6-sulfate copolymer was sutured to the posterior wall of each artery. Animals were killed at intervals of up to 3 months. All arteries remained patent. By 24 hours the membrane had become infiltrated with fibrin and red blood cells. An inflammatory response ensued and by 8 days the membrane was filled with mononuclear cells. At 3 months only a small remnant of the membrane remained. Intimal hyperplasia developed throughout the injured aorta. However, the hyperplastic response beneath the membrane was no greater than that observed in the adjacent injured aorta. A bioresorbable membrane can be sutured into the lumen of a small-diameter vessel without inducing thrombosis and without locally increasing intimal hyperplasia. A prosthesis of this type might be used to deliver inhibitors of smooth muscle cell proliferation and migration to the injured arterial wall.
KeywordsSmooth Muscle Cell Zealand White Rabbit Intimal Hyperplasia Smooth Muscle Cell Proliferation Collagen Membrane
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- 1.Imparato AM, Braceo A, Kim GE, et al. Intimal and neointimal fibrous proliferation causing failure of arterial reconstruction. Surgery 1972;72:1007–1017.Google Scholar
- 2.Donaldson MC, Mannick JA, Whittemore AD. Causes of primary graft failure after in situ vein bypass grafting. J Vasc Surg 1992;15:113–120.Google Scholar
- 3.Majack RA, Clowes AW. Inhibition of vascular smooth muscle cell migration by heparin-like glycosaminoglycans. J Cell Physiol 1984; 118:253–256.Google Scholar
- 4.Powell JS, Clozel JP, Muller RK, et al. Inhibitors of angiotensin-converting enzyme prevent myointimal proliferation after vascular injury. Science 1989;245:186–188.Google Scholar
- 5.Chervu A, Moore WS, Quinones-Baldrich WJ, et al. Efficacy of corticosteroids in suppression of intimal hyperplasia. J Vasc Surg 1989;10:129–134.Google Scholar
- 6.Clowes AW, Clowes MM. Kinetics of cellular proliferation after arterial injury. IV heparin inhibits rat smooth muscle mitogenesis and migration. Circ Res 1986:58:839–845.Google Scholar
- 7.Yannas IV, Burke JF, Orgill DP, et al. Wound tissue can utilize a polymeric template to synthesize a functional extension of skin. Science 1982;215:174–176.Google Scholar
- 8.Lundborg G, Gelberman RH, Longo FM, et al. In vivo regeneration of cut nerves encased in silicone tubes. J Neuropathol Exp Neurol 1982;41:412–422.Google Scholar
- 9.Silver FH, Yannas IV, Salzman EW. Glycosaminoglycan inhibition of collagen induced platelet aggregation. Thromb Res 1978;13:267–277.Google Scholar
- 10.Edelman ER, Adams DH, Karnovsky MJ. Effect of controlled adventitial heparin delivery on smooth muscle cell proliferation following endothelial injury. Proc Natl Acad Sci 1990; 87:3773–3777.Google Scholar
- 11.Simons M, Edelman ER, DeKeyser JL, et al. Antisense c-myb oligonucleotides inhibit intimai arterial smooth muscle cell accumulation in vivo. Nature 1992;359:67–70.Google Scholar