The neointima formed in endothelial cell sodded ePTFE vascular grafts results from both cellular-hyperplasia and extracellular-hypertrophy.
Endothelial cell transplantation onto polymeric vascular grafts results in the formation of a neointima. The formation of this neointima is often suggested to result from a chronic cellular hyperplasia where the terms intimal hyperplasia and intimal thickening are used interchangeably. While the formation of a midgraft neointima in sodded grafts involves a level of cell proliferation, the synthesis and deposition of extracellular matrix proteins is also a ubiquitous observation in these grafts. To assess the composition of midgraft neointima in sodded grafts, a morphometric method was developed to provide a differential quantitation of the cellular-hyperplastic and extracellular-hypertrophic elements of intimal thickening. The formed neointima on microvessel endothelial cell sodded and control (noncell-treated) ePTFE vascular grafts was quantified after 3, 12, and 52 wk of graft implantation in a canine carotid artery model. Midgraft sections of grafts were evaluated for both intimal thickness (IT) and cell density per unit volume and quantified using a PC-based image analysis program. Sodded grafts explanted at 3 wk exhibited an average neointimal cell density (3 x 10(9) cells/cm3; IT 30 microns) equivalent to cell densities observed in normal arterial media. After 12 wk the mean cell density approached a hyperplastic value (3.7 x 10(9) cells/cm3; IT 76 microns), while grafts explanted after 52 wk exhibited a mean cell density (2.8 x 10(9) cells/cm3; IT 30 microns) similar to 3-wk values. Control grafts that received no cells exhibited no midgraft cellular coverage. These results indicate that neointima formation in the midgraft region of sodded grafts occurred via mechanisms involving both a cellular hyperplasia and an extracellular hypertrophy. Differential responses occur presumably due to localized differences in cellular proliferation and cellular biosynthetic activity.
Kleinert
L B
LB
Department of Surgery, University of Arizona, Tucson 85724, USA.
Hoying
J B
JB
Williams
S K
SK
D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D002339:Carotid Arteries / Q000166:cytology* / Q000473:pathology; D017690:Cell Transplantation / Q000295:instrumentation / Q000379:methods; D004176:Dipyridamole / Q000494:pharmacology; D004285:Dogs; D004730:Endothelium, Vascular / Q000637:transplantation*; D006965:Hyperplasia; D006984:Hypertrophy; D008833:Microcirculation; D009389:Neovascularization, Pathologic; D018919:Neovascularization, Physiologic; D011138:Polytetrafluoroethylene; D017539:Tunica Intima / Q000166:cytology* / Q000473:pathology; D014656:Vascular Surgical Procedures / Q000379:methods*
D004176:Dipyridamole; D011138:Polytetrafluoroethylene; D001241:Aspirin