title: Experimental macular edema induced by macular venule occlusion in monkey.
abstract: OBJECTIVE
  Visual prognosis after retinal vein occlusion varies, because it may be affected by macular edema or an avascular area. The mechanism describing how macular edema and avascular areas occur, however, has not been clearly understood. We induced macular edema in cynomolgus monkeys by occluding macular venules to evaluate the retinal microcirculation.
  
  
  METHODS
  We produced venous occlusion by applying dye laser in three cynomolgus monkeys. Macular edema was examined by slit lamp biomicroscopy and optical coherence tomography. Acridine orange leukocyte fluorography (AOLF) and fluorescein angiography were performed to study blood flow and vascular leakage before and after laser application.
  
  
  RESULTS
  We observed three types of retinal changes in the macular area: (1) macular edema did not develop; (2) macular edema developed, but improved with avascular area formation; (3) macular edema developed, but disappeared without avascular area formation. Under physiological conditions, observation revealed that leukocytes flowed from arterioles into either superior or inferior venules. When macular edema did not develop, most leukocytes from arterioles escaped into the adjacent non-occluded venules. In contrast, when macular edema occurred, leukocyte flow became stagnated. Macular edema developed when capillary leakage was observed from venules and subsequently arterioles, but disappeared when an avascular area was formed by arteriole occlusion.
  
  
  CONCLUSIONS
  We demonstrated that experimental macular edema could be induced by macular venule occlusion in monkeys. According to our observation by AOLF, whether macular edema is induced or not depends on the function of collateral routes of the remaining non-occluded venules. We could consider that a gradual increase in intravascular pressure was associated with the avascular area formation.
authors.affiliation: Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Ieki
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Nishiwaki
authors.forename: Shinji
authors.initials: S
authors.lastname: Miura
authors.forename: Kenji
authors.initials: K
authors.lastname: Yamashiro
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Nishijima
authors.forename: Atsushi
authors.initials: A
authors.lastname: Nonaka
authors.forename: Junichi
authors.initials: J
authors.lastname: Kiryu
authors.forename: Yoshihito
authors.initials: Y
authors.lastname: Honda
mesh_terms: D000165:Acridine Orange; D000818:Animals; D001783:Blood Flow Velocity; D004195:Disease Models, Animal; D005451:Fluorescein Angiography; D005456:Fluorescent Dyes; D007368:Interferometry; D017075:Laser Coagulation; D007962:Leukocytes / Q000502:physiology; D008027:Light; D008252:Macaca fascicularis; D008269:Macular Edema / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D012169:Retinal Vein / Q000601:surgery; D012170:Retinal Vein Occlusion / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology; D012171:Retinal Vessels / Q000502:physiology; D014054:Tomography; D014699:Venules
chemical_list: D005456:Fluorescent Dyes; D000165:Acridine Orange