December 1997
Volume 38, Issue 13
Free
Articles  |   December 1997
The effect of acute experimental retinal vein occlusion on cat retinal vein pressures.
Author Affiliations
  • R Attariwala
    Biomedical Engineering Department, Northwestern University, Evanston, Illinois 60201-3107, USA.
  • P S Jensen
    Biomedical Engineering Department, Northwestern University, Evanston, Illinois 60201-3107, USA.
  • M R Glucksberg
    Biomedical Engineering Department, Northwestern University, Evanston, Illinois 60201-3107, USA.
Investigative Ophthalmology & Visual Science December 1997, Vol.38, 2742-2749. doi:
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      R Attariwala, P S Jensen, M R Glucksberg; The effect of acute experimental retinal vein occlusion on cat retinal vein pressures.. Invest. Ophthalmol. Vis. Sci. 1997;38(13):2742-2749.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

PURPOSE: Retinal ischemic damage associated with retinal vein occlusion is exacerbated by fluid extravasation and hemorrhage, which may be caused by increased permeability, elevated intravascular pressure, or both. Direct measurement of the retinal vein pressure in the cat after acute experimental retinal vein occlusion may define the role of intravascular pressures in fluid extravasation associated with this condition. METHODS: Intravenous retinal pressure measurements were obtained using a micropipette connected to a servonull device and positioned by a robot micromanipulator, while a major retinal vein near the optic disc was occluded by argon laser radiation delivered through an optical fiber positioned by a manual micromanipulator. After occlusion, retinal vein pressures were measured on both sides of the occlusion site at a controlled intraocular pressure of 20 mm Hg. RESULTS: Upstream of the occlusion site, the retinal vein pressures were not greatly elevated, although they were significantly different from controls. Downstream vein pressures were significantly lower than controls, but vascular collapse near the optic nerve was not observed. CONCLUSIONS: In retinal vein occlusion, venous pressures in a segmental retinal circulatory bed are not substantially elevated, thus implying the presence of a pressure-release mechanism and implicating vascular damage for the increased transvascular fluid flux. The lack of vascular collapse downstream of the occlusion site suggests collateral communication before a large intraocular pressure-dependent resistance segment that lies between the intraocular and extraocular vessels.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×