Adaptive remodeling of internal elastic lamina and endothelial lining during flow-induced arterial enlargement

Gaps in the internal elastic lamina (IEL) have been observed in arteries ex posed to high blood flow. To characterize the nature and consequences of th is change, blood flow was increased in the carotid arteries of 56 adult, ma le, Japanese white rabbits by creating an arteriovenous fistula between the common carotid artery and the external jugular vein. The common carotid ar tery proximal to the arteriovenous fistula was studied at intervals from 1 hour to 8 weeks after exposure to high flow. In the controls, the IEL showe d only the usual, small, physiological holes, 2 to 10 mu m in diameter. At 3 days, some of the holes in the IEL had become enlarged, but they could no t be detected by scanning electron microscopy, despite manifest endothelial cell proliferation. At 4 days, gaps in the IEL appeared as small, luminal surface depressions, 15 to 50 mu m wide. At 7 days, the gaps in the IEL had enlarged and formed circumferential, luminal depressions occupying 15+/-5% of the lumen surface. Endothelial cell proliferation persisted in the gaps while proliferative activity decreased where the IEL remained intact. At 4 weeks, as the artery became elongated and dilated,the gaps in the IEL wide ned as intercommunicating circumferential and longitudinal luminal depressi ons occupying 64+/-5% of the lumen surface. At 8 weeks, the rate of elongat ion and dilatation of the artery slowed and the widening of the gaps in the IEL diminished. Endothelial cells covered the gaps throughout. We conclude that flow-induced arterial dilatation is accompanied by an adaptive remode ling of the intima. The gaps in the IEL permit an increase in lumen surface area while endothelial cell proliferation assures a continuous cell lining throughout.