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The Journal of Thoracic and Cardiovascular Surgery, Vol 79, 911-915, Copyright © 1980 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
LI Bonchek
Abundant experimental evidence indicates that damage to vascular
endothelium decreases intimal fibrinolytic activity, causes mural platelet
and fibrin deposition, encourages proliferation of the exposed subintimal
fibrocytes and smooth muscle cells, and increases endothelial permeability.
These processes lead to thrombosis, subendothelial hyperplasia, or
accelerated atherosclerosis. We have demonstrated in monkeys that
distention of veins at high pressures (700 mm Hg), as commonly done
clinically in preparation for coronary bypass, causes severe damage to the
endothelium (as seen by scanning electron microscopy), and increased lipid
uptake by the vein wall. The endothelium of veins distended at lower
pressures (300-400 mm Hg) was not significantly different from that of
undistended veins. Because of the potential late consequences of early
endothelial damage to vein grafts, distention of veins before grafting to
overcome spasm and to identify leaks must be done at controlled pressures.
A convenient balloon device has been developed which limits the maximum
pressure that can be applied when the vein is dilated.
ARTICLES
Prevention of endothelial damage during preparation of saphenous veins for bypass grafting
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