title: Diabetic macular edema: passive and active transport of fluorescein through the blood-retina barrier.
abstract: OBJECTIVE
  To investigate the passive bidirectional and active outward transport of fluorescein through the blood-retina barrier (BRB) in diabetic patients with clinically significant macular edema and in healthy controls.
  
  
  METHODS
  The passive and active transport of fluorescein through the BRB was quantitated by vitreous fluorometry. A previously developed method was used to model passive transport. A new simulation model was developed and evaluated for estimation of active transport. The study included 10 eyes of 5 healthy controls and 31 eyes of 20 diabetic patients with clinically significant diabetic macular edema (CSME) in at least one eye, totalling 25 eyes with CSME.
  
  
  RESULTS
  Passive permeability of fluorescein was increased by a factor of 12 in eyes with edema compared to healthy controls (edema, 23.7 nm/sec; healthy subjects, 1.9 nm/sec, P < 0.01), whereas the active transport was doubled (edema, 84.1 nm/sec; healthy subjects, 43.5 nm/sec, P < 0.01). Unlike active transport, passive permeability was related to the degree of retinopathy, in that eyes with severe non-proliferative diabetic retinopathy had a passive permeability that was significantly increased compared to moderate retinopathy (32.1 nm/sec and 14.6 nm/sec, respectively, P: < 0.05). The passive movement quantitated with vitreous fluorometry was larger for diffuse and mixed leakage compared to focal (P = 0.07).
  
  
  CONCLUSIONS
  Insofar as the movement of fluorescein can be taken as a probe for the movement of electrolytes and water, the pathogenesis of diabetic macular edema seems to involve a disruption of the BRB, presumably its inner component. The active resorptive functions of the blood-retina barrier appear to be compensatorily increased to counteract edema formation, although the increase is too small to prevent edema in the face of severe leakage through the blood-retina barrier.
authors.affiliation: Department of Ophthalmology, Herlev Hospital, University of Copenhagen, Denmark. bsander@idea.dk
authors.forename: B
authors.initials: B
authors.lastname: Sander
authors.forename: M
authors.initials: M
authors.lastname: Larsen
authors.forename: B
authors.initials: B
authors.lastname: Moldow
authors.forename: H
authors.initials: H
authors.lastname: Lund-Andersen
mesh_terms: D000328:Adult; D000368:Aged; D001693:Biological Transport, Active; D001813:Blood-Retinal Barrier; D002199:Capillary Permeability; D003198:Computer Simulation; D003930:Diabetic Retinopathy / Q000378:metabolism*; D019793:Fluorescein / Q000378:metabolism*; D015590:Fluorophotometry; D005654:Fundus Oculi; D006801:Humans; D008269:Macular Edema / Q000378:metabolism*; D008875:Middle Aged; D010781:Photography
chemical_list: D019793:Fluorescein