Application of coacervated alpha-elastin to arterial prostheses for inhibition of anastomotic intimal hyperplasia.

Prevention of anastomotic intimal hyperplasia (AIH) requires inhibition of the migration of smooth muscle cells (SMCs) and promotion of endothelial cell (ECs) growth from the native arterial wall. We investigated the effect of coacervated alpha-elastin on migration of SMCs and ECs in vitro. SMCs and ECs were prepared from porcine aortic media and endothelium. Coacervated alpha-elastin was coated and cross-linked around the perimeter of each 1 cm diameter center of a well in a 12 well plate. SMCs and ECs were placed and cultured within the center of each well. The migration of SMCs and ECs on coacervated alpha-elastin was assayed on the second, third (10 mg/ml), or fourth day (0.1, 1.0, 10.0 mg/ml) of cultivation by measuring the area of migration from the 1 cm diameter center. Coacervated alpha-elastin was then coated and cross-linked on a Dacron graft using 1% glycerol polyglycidyl ether (GPGE) and examined with scanning electron microscopy to determine the feasibility of graft coating. SMC migration was significantly inhibited dose dependently over time (p < 0.005), e.g., 0.1 mg/ml (45.4% +/- 2.7%: % of MES [pH 5] and 1% GPGE without alpha-elastin), 1.0 mg/ml (32.0% +/- 1.4%), 10.0 mg/ml (8.3% +/- 2.9%). EC migration (90.7% +/- 6.2%: p = ns) was not inhibited by 0.1 mg/ml of coacervated alpha-elastin. Cross-linked coacervated alpha-elastin was coated on a dacron graft uniformly. Incorporation of coacervated alpha-elastin into the structure of arterial prostheses offers the possibility of inhibition of SMC hyperplasia without inhibition of EC formation.