title: A new kind of labyrinth-like capillary is responsible for leakage from human choroidal neovascular endothelium, as investigated by high-resolution electron microscopy.
abstract: OBJECTIVE
  This study reports the clinicopathologic findings of leaky sites in pathological vessels after submacular removal of choroidal neovascular membranes (CNV). As the site that causes fluid exudation from neovascular vessels is unknown, specific attention was focused on the formation of fenestrations, cellular junctions, and morphologic alteration which can cause endothelial leakage.
  
  
  METHODS
  Choroidal neovascular membranes of 15 patients who underwent submacular surgery for CNV were investigated. Five patients received bevacizumab treatment before surgery, and another five received photodynamic therapy before surgery. The remaining five did not receive any other treatment before surgery. All membranes were embedded for transmission electron microscopy. CNVs were analyzed for pathological cell-to-cell connections, fenestrations, or other pathological conditions which can cause leakage of plasma.
  
  
  RESULTS
  The morphology of the newly formed blood channels was very variable, and in principle was not different in treated and untreated patients. The sources of leakage in neovascular choroidal vessels were caused by insufficient endothelial cell connections and by capillaries with microvillar projections into the vessel lumen which blocked cellular perfusion but still allowed the flow of plasma. Fenestrations were only infrequently observed.
  
  
  CONCLUSIONS
  A newly discovered type of pathological capillary, called a labyrinth capillary, is very likely responsible for the permanent leakage of fluid. Due to the small vessel lumen, thrombocytes cannot enter these capillaries to close the leakages. Fenestrations did not appear to play a significant role in vascular leakiness.
authors.affiliation: Vitreoretinal Surgery, Centre for Ophthalmology, Schleichstrasse 12/1, 72076, Tuebingen, Germany, Ulrich.Schraermeyer@med.uni-tuebingen.de.
authors.forename: Ulrich
authors.initials: U
authors.lastname: Schraermeyer
authors.forename: Sylvie
authors.initials: S
authors.lastname: Julien
authors.forename: Antje
authors.initials: A
authors.lastname: Biesemeier
authors.forename: Karl Ulrich
authors.initials: KU
authors.lastname: Bartz-Schmidt
authors.forename: Hartwig
authors.initials: H
authors.lastname: Wolburg
mesh_terms: D000369:Aged, 80 and over; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D000068258:Bevacizumab; D002196:Capillaries / Q000648:ultrastructure*; D002199:Capillary Permeability; D002829:Choroid / Q000098:blood supply*; D020256:Choroidal Neovascularization / Q000188:drug therapy / Q000473:pathology*; D004730:Endothelium, Vascular / Q000648:ultrastructure*; D006801:Humans; D058449:Intravitreal Injections; D046529:Microscopy, Electron, Transmission; D010778:Photochemotherapy; D012189:Retrospective Studies; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors; D057135:Wet Macular Degeneration / Q000188:drug therapy / Q000473:pathology
chemical_list: D020533:Angiogenesis Inhibitors; D061067:Antibodies, Monoclonal, Humanized; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab