April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Systemic Brimonidine is Neuroprotective in OHT-Induced RGC Apoptosis in vivo
Author Affiliations & Notes
  • S. Nizari
    Glaucoma & Retinal Neurodegeneration Research Group, UCL Institute of Ophthalmology, London, United Kingdom
  • L. Guo
    Glaucoma & Retinal Neurodegeneration Research Group, UCL Institute of Ophthalmology, London, United Kingdom
  • M. F. Cordeiro
    Glaucoma & Retinal Neurodegeneration Research Group, UCL Institute of Ophthalmology, London, United Kingdom
    Glaucoma Research Unit, Western Eye Hospital, London, United Kingdom
  • Footnotes
    Commercial Relationships  S. Nizari, None; L. Guo, None; M.F. Cordeiro, Allergan, F; Sooft, Allergan, Visufarma, R.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 3185. doi:https://doi.org/
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      S. Nizari, L. Guo, M. F. Cordeiro; Systemic Brimonidine is Neuroprotective in OHT-Induced RGC Apoptosis in vivo. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3185. doi: https://doi.org/.

      Download citation file:


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

      ×
  • Supplements
Abstract
 
Purpose:
 

Brimonidine (BMD) has been shown to be neuroprotective via a number of different mechanisms. It is used topically in glaucoma for lowering intraocular pressure, although this effect is believed to be limited on systemic administration. Here, we investigate intraperitoneal BMD and RGC apoptosis in a rat model of ocular hypertension.

 
Methods:
 

Using our established chronic ocular hypertension (OHT) rat model, IOP was induced in 36 animals, with DARC imaging performed at 3 and 8 weeks after IOP elevation. Animals were randomly assigned to no treatment (untreated OHT) or intraperitoneal BMD (0.1 mg/kg) at singly time of IOP elevation (single, BMD) or multiple doses at surgery and 1 & 2 weeks later (multiple, BMD). The IOP of both eyes in each rat was measured regularly using a Tonolab pen. Mean values were calculated with 95% confidence intervals for the absolute counts. All treatment groups were compared to each other and control using ANOVA. The percentage reduction in RGC apoptosis associated with treatment and compared to control were calculated, as we have previously described.

 
Results:
 

Both single and multiple BMD treatments induced a significant reduction in RGC apoptosis at 3 and 8 weeks after IOP elevation compared to control (p<0.001). Interestingly there was no difference between single or multiple treatment regimens at either time point. There was no statistical difference between IOPs between treatment groups.

 
Conclusions:
 

Systemic brimonidine treatment appears to very effectively inhibit RGC apoptosis in our experimental OHT model, and its effects are not related to intraocular pressure. More importantly, its effect is prolonged, with efficacy demonstrable even after 8 weeks with a single application. Our results are consistent with previous published results, the most recent being from Hernandez et al , who showed a non-IOP dependent neuroprotective effect of systemic brimonidine in an experimental model of OHT.

 
References:
 

M. Hernandez et al, Experimental Eye Research 86 (2008) 798-806.  

 
Keywords: neuroprotection • apoptosis/cell death • ganglion cells 
×
×

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.

×