title: Inflammatory response after scatter laser photocoagulation in nonphotocoagulated retina.
abstract: OBJECTIVE
  Macular edema is one of the most serious adverse effects after retinal scatter laser photocoagulation. It has been suggested that the changes in the distribution of retinal blood flow or the inflammatory reaction after photocoagulation may be involved in the pathogenesis of macular edema, but little information is available about its exact mechanism. This study was designed to evaluate quantitatively leukocyte-endothelial cell interactions and vascular permeability in the nonphotocoagulated portions of the retina after partial scatter laser photocoagulation.
  
  
  METHODS
  Argon laser photocoagulation was performed in one half of the retina in male pigmented rats (n = 90). In the other half of the retina, leukocyte dynamics after photocoagulation were evaluated in vivo with acridine orange digital fluorography. Retinal vessel permeability was quantified by using Evans blue dye.
  
  
  RESULTS
  Scatter laser photocoagulation caused significant inflammatory leukocyte-endothelial interactions not only in the photocoagulated but also in the untreated half of the retina. In the nonphotocoagulated half of the retina, the number of leukocytes rolling along the major retinal veins increased after photocoagulation and peaked at 12 hours (14.3 +/- 4.5 cells/min per vessel). Leukocyte accumulation in the untreated half of the retina increased after photocoagulation, with a peak of 47.5 +/- 13.0 cells/mm(2) 24 hours after photocoagulation. Retinal vascular permeability in the untreated half of the retina gradually increased after photocoagulation.
  
  
  CONCLUSIONS
  Scatter laser photocoagulation increased leukocyte rolling and subsequent accumulation in both the photocoagulated and the untreated portions of the retina. The accumulated leukocytes may be involved in the augmented vascular permeability in the untreated retina, resulting in retinal edema after photocoagulation.
authors.affiliation: Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Nonaka
authors.forename: Junichi
authors.initials: J
authors.lastname: Kiryu
authors.forename: Akitaka
authors.initials: A
authors.lastname: Tsujikawa
authors.forename: Kenji
authors.initials: K
authors.lastname: Yamashiro
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Nishijima
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kamizuru
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Ieki
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Miyamoto
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Nishiwaki
authors.forename: Yoshihito
authors.initials: Y
authors.lastname: Honda
authors.forename: Yuichiro
authors.initials: Y
authors.lastname: Ogura
mesh_terms: D000165:Acridine Orange; D000818:Animals; D002199:Capillary Permeability; D002465:Cell Movement; D004730:Endothelium, Vascular / Q000378:metabolism; D005070:Evans Blue; D005456:Fluorescent Dyes; D007091:Image Processing, Computer-Assisted; D017075:Laser Coagulation / Q000009:adverse effects*; D007958:Leukocyte Count; D007962:Leukocytes / Q000502:physiology; D008269:Macular Edema / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D008297:Male; D051381:Rats; D020318:Rats, Long-Evans; D012160:Retina / Q000601:surgery*; D012171:Retinal Vessels / Q000378:metabolism / Q000473:pathology; D012173:Retinitis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology
chemical_list: D005456:Fluorescent Dyes; D005070:Evans Blue; D000165:Acridine Orange