title: Arterial intimal-medial permeability and coevolving structural responses to defined shear-stress exposures.
abstract: The purpose of this research was to examine the evolution of arterial shear stress-induced intimal albumin permeability and coevolving structural responses in swine arteries. Uniform laminar shear-stress responses were compared with those of a simulated "flow separation" stress field. These fields were created using specially designed flow-configuring devices in an experimentally controlled, metabolically supported, ex vivo thoracoabdominal aorta preparation. The Evans blue dye-albumin complex (EBD-alb) permeability patterns that evolved were measured by a reflectometric method. The corresponding tissue structural responses were evaluated by histological, immunostaining, and ultrastructural microscopic techniques. It was shown that when a previously in vivo-adapted artery is challenged by a new mechanochemical environment, it undergoes a sequence of adaptive processes over the ensuing 95 h. Intimal regions of laminar shear-stress exposure ( approximately 16 dyn/cm(2)) responded initially (23 h) with an increase in permeability. With continued stress exposure, intimal-medial structural changes ensued that restored the artery to a physiologically normal permeability. Over this same period, adjacent endothelial regions exposed to simulated flow separation stress fields ( approximately 0.03-0.27 dyn/cm(2)) developed early and progressively increasing permeability. This was associated with formation of local intimal edema, loss of intimal matrix material, and development of distinctively raised, gelatinous-appearing intimal lesions having a potentially preatheromatous architecture.
authors.affiliation: Laboratory of Experimental Atherosclerosis, Department of Internal Medicine, College of Medicine, Ohio State University, Columbus 43210, USA. fry.1@osu.edu
authors.forename: Donald L
authors.initials: DL
authors.lastname: Fry
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology / Q000502:physiology*; D001161:Arteriosclerosis / Q000209:etiology; D046508:Culture Techniques / Q000295:instrumentation; D004730:Endothelium, Vascular / Q000166:cytology / Q000502:physiology / Q000648:ultrastructure; D005070:Evans Blue / Q000493:pharmacokinetics; D005260:Female; D020342:Finite Element Analysis; D006439:Hemodynamics / Q000502:physiology*; D018056:Hemorheology / Q000295:instrumentation / Q000379:methods*; D008297:Male; D008955:Models, Cardiovascular; D019001:Nitric Oxide Synthase / Q000096:biosynthesis; D052250:Nitric Oxide Synthase Type III; D010477:Perfusion; D010539:Permeability; D010587:Phagocytosis / Q000502:physiology; D012709:Serum Albumin / Q000493:pharmacokinetics; D013314:Stress, Mechanical; D013552:Swine; D017539:Tunica Intima / Q000166:cytology / Q000502:physiology*; D017540:Tunica Media / Q000166:cytology / Q000502:physiology*
chemical_list: D012709:Serum Albumin; D005070:Evans Blue; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III