title: Adaptive remodeling of internal elastic lamina and endothelial lining during flow-induced arterial enlargement.
abstract: Gaps in the internal elastic lamina (IEL) have been observed in arteries exposed to high blood flow. To characterize the nature and consequences of this change, blood flow was increased in the carotid arteries of 56 adult, male, Japanese white rabbits by creating an arteriovenous fistula between the common carotid artery and the external jugular vein. The common carotid artery 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 showed only the usual, small, physiological holes, 2 to 10 microm in diameter. At 3 days, some of the holes in the IEL had become enlarged, but they could not 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 microm 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 widened as intercommunicating circumferential and longitudinal luminal depressions occupying 64+/-5% of the lumen surface. At 8 weeks, the rate of elongation 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 remodeling 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.
authors.affiliation: Second Department of Pathology, Akita University School of Medicine, Hondo, Japan. masuda@med.akita-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Masuda
authors.forename: Y J
authors.initials: YJ
authors.lastname: Zhuang
authors.forename: T M
authors.initials: TM
authors.lastname: Singh
authors.forename: K
authors.initials: K
authors.lastname: Kawamura
authors.forename: M
authors.initials: M
authors.lastname: Murakami
authors.forename: C K
authors.initials: CK
authors.lastname: Zarins
authors.forename: S
authors.initials: S
authors.lastname: Glagov
mesh_terms: D000818:Animals; D000963:Antimetabolites / Q000378:metabolism / Q000494:pharmacology; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001973:Bromodeoxyuridine / Q000378:metabolism / Q000494:pharmacology; D017536:Carotid Artery, Common / Q000473:pathology / Q000502:physiology* / Q000648:ultrastructure; D002452:Cell Count; D002455:Cell Division / Q000502:physiology; D004547:Elastic Tissue / Q000473:pathology / Q000502:physiology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000502:physiology* / Q000648:ultrastructure; D008297:Male; D008855:Microscopy, Electron, Scanning; D009131:Muscle, Smooth, Vascular / Q000473:pathology / Q000502:physiology / Q000648:ultrastructure; D011817:Rabbits; D014664:Vasodilation / Q000502:physiology*
chemical_list: D000963:Antimetabolites; D001973:Bromodeoxyuridine