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The Journal of Thoracic and Cardiovascular Surgery, Vol 103, 1093-1103, Copyright © 1992 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
GD Angelini, AJ Bryan, HM Williams, AA Soyombo, A Williams, J Tovey and AC Newby
With use of an established model of pig saphenous vein grafts in the
carotid artery, the time-course of the following changes was related: (1)
medial and intimal size by morphometry of transverse sections, (2) cell
number by deoxyribonucleic acid concentration, (3) cell density by
deoxyribonucleic acid concentration per milligram wet weight and by
counting nuclei in transverse sections, (4) endothelial morphology by
scanning electron microscopy, and (5) cholesterol concentration. In the
first week after grafting, medial and intimal thickening occurred
associated with an increase in cell number. Between 1 and 4 weeks after
grafting, further rapid medial and intimal thickening occurred with no
further increase in cell number but with a reduction in cell density, which
suggested that cell migration, hypertrophy, and the laying down of
extracellular matrix were responsible. Between 4 and 39 weeks after
grafting, a slower increase in medial and intimal size occurred, associated
with a parallel increase in cell number and no further change in cell
density. The endothelium of grafts showed only localized abnormalities,
including loss of cells and leukocyte adhesion, either 1 or 4 weeks after
grafting. Cholesterol concentration was slightly elevated 1 week after
grafting but returned to values similar to those in vein by 4 weeks after
grafting. Distention to 600 mm Hg during surgical preparation of vein for
grafting resulted in lower graft patency after either 1 or 4 weeks and
caused significant medial and endothelial injury. Distention did not,
however, affect changes in medial or intimal size, deoxyribonucleic acid,
or cholesterol concentration caused by grafting. We conclude that three
processes contribute to medial and intimal thickening, namely: (1) an
initial phase of rapid smooth muscle cell proliferation, (2) smooth muscle
cell migration, hypertrophy, and synthesis of extracellular matrix, and (3)
a late phase of slower smooth muscle cell proliferation. The incomplete
late suppression of smooth muscle cell proliferation occurs despite
regeneration of a morphologically intact endothelium and in the absence of
progressive cholesterol accumulation.
ARTICLES
Time-course of medial and intimal thickening in pig venous arterial grafts: relationship to endothelial injury and cholesterol accumulation
Department of Cardiology, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom.
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S. E. Francis, S. Hunter, C. M. Holt, P. A. Gadsdon, S. Rogers, G. W. Duff, A. C. Newby, and G. D. Angelini Release of platelet-derived growth factor activity from pig venous arterial grafts J. Thorac. Cardiovasc. Surg., September 1, 1994; 108(3): 540 - 548. [Abstract] [Full Text]
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