title: Ultrastructure of endothelial cells under flow alteration.
abstract: Endothelial cells are stable and quiet in normal animals. They arrange regularly and have a smooth lumen surface and thin endothelial wall. According to Thoma's principle (1893) and Kamiya and Togawa's principle (1980) on the relationship of the vascular diameter to flow alteration, blood flow is in equilibrium to the diameter and in a physiological state. That is to say, there is no fast flow or slow flow. To understand the nature of the endothelial cells, we should investigate endothelial cells under flow alteration to break the equilibrium state. Endothelial cells under increased flow were studied in arteries with an arteriovenous fistula or in the capillaries of myocardium with volume-overloaded hearts or of the skeletal muscle by electrical stimulation. Those under decreased flow were studied by the closure of the fistula or by ceasing the stimulation. Endothelial cells in the coarctation of the arteries were also observed. Endothelial cells were activated by increased flow in the arteries and capillaries, while they were inactivated by decreased flow. Endothelial activation is characterized as lumen protrusions, increase of cytoplasmic organelles, abluminal protrusions, basement membrane degradation, internal elastic lamina degradation in the arteries, and sproutings in the capillaries. These are ultrastructurally comparable to angiogenesis. Endothelial inactivation is characterized by the decrease of endothelial cell number with apoptosis, which is ultrastructurally comparable to angioregression. We assume that endothelial cells respond to increased flow by angiogenesis and to decreased flow by angioregression.
authors.affiliation: Second Department of Pathology, Akita University School of Medicine, Akita 010-8543, Japan. masuda@med.akita-u.ac.jp
authors.forename: Hirotake
authors.initials: H
authors.lastname: Masuda
authors.forename: Koichi
authors.initials: K
authors.lastname: Kawamura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nanjo
authors.forename: Eiketsu
authors.initials: E
authors.lastname: Sho
authors.forename: Masayo
authors.initials: M
authors.lastname: Komatsu
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Sugiyama
authors.forename: Akihiro
authors.initials: A
authors.lastname: Sugita
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Asari
authors.forename: Mikio
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Toshihito
authors.initials: T
authors.lastname: Ebina
authors.forename: Naoto
authors.initials: N
authors.lastname: Hoshi
authors.forename: Tej M
authors.initials: TM
authors.lastname: Singh
authors.forename: Chengpei
authors.initials: C
authors.lastname: Xu
authors.forename: Christopher K
authors.initials: CK
authors.lastname: Zarins
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity; D002196:Capillaries / Q000503:physiopathology; D017536:Carotid Artery, Common / Q000503:physiopathology; D003326:Coronary Circulation / Q000502:physiology; D004285:Dogs; D004730:Endothelium, Vascular / Q000166:cytology / Q000503:physiopathology* / Q000648:ultrastructure*; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D011817:Rabbits; D051381:Rats