May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Extracellular Carbonic Anhydrase I (CA–I) Induces Retinal Leukocyte Adhesion and Alters Electrophysiology in Non–Diabetic Rat
Author Affiliations & Notes
  • D.K. Bursell
    Beetham, Joslin Diabetes Center, Boston, MA
  • A.C. Clermont
    Beetham, Joslin Diabetes Center, Boston, MA
  • G. Terrero
    Beetham, Joslin Diabetes Center, Boston, MA
  • B. Gao
    Beetham, Joslin Diabetes Center, Boston, MA
  • S. Rook
    Beetham, Joslin Diabetes Center, Boston, MA
  • L.P. Aiello
    Beetham, Joslin Diabetes Center, Boston, MA
  • E.P. Feener
    Beetham, Joslin Diabetes Center, Boston, MA
  • S.–E. Bursell
    Beetham, Joslin Diabetes Center, Boston, MA
  • Footnotes
    Commercial Relationships  D.K. Bursell, None; A.C. Clermont, None; G. Terrero, None; B. Gao, None; S. Rook, None; L.P. Aiello, None; E.P. Feener, None; S. Bursell, None.
  • Footnotes
    Support  Massachusetts Lions
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 3764. doi:
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      D.K. Bursell, A.C. Clermont, G. Terrero, B. Gao, S. Rook, L.P. Aiello, E.P. Feener, S.–E. Bursell; Extracellular Carbonic Anhydrase I (CA–I) Induces Retinal Leukocyte Adhesion and Alters Electrophysiology in Non–Diabetic Rat . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3764.

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

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Abstract

Purpose: : Carbonic anhydrase (Ca) enzymes are known to regulate cellular acid base homeostasis, membrane ion transport, and fluid movement. Intravitreal injection of Ca–I in vivo has been shown to increase retinal vascular permeability (RVP). This study examines whether Ca–I also has an impact on other markers for early diabetes associated retinal dysfunction such as increased retinal leukostasis and electrophysiological abnormalities.

Methods: : Intravitreal injections (10µL) of CA–I (200ng), CA–I + acetazolamide (10µM), or balanced saline solution (BSS) were performed under sterile conditions in male Sprague–Dawley rats. At 1 or 48 hours post injection, leukocyte adhesion was assessed by acridine orange (1mg/kg in sterile saline) infusion. Static leukocytes were imaged by scanning laser ophthalmoscope at 20 minutes post infusion and quantified across 9 quadrants. Electroretinograms (ERG) (single white flash, 1.4x10^4 ftc, 5 ms) were obtained from both eyes after 1 hour of dark adaptation.

Results: : Intravitreal CA–I did not effect leukostasis at 1 hour after injection. At 48 hours post injection, CA–I induced a 3–fold increase in retinal leukostasis compared to BSS treated eyes (13.8±4.5 vs 4.4±1.6 cells/pixel2, p<0.001). The increase in retinal leukostasis by CA–I was inhibited with co–injection with acetazolamide (4.8±1.3, p<0.001). The injection of Ca–I shortened implicit time for the a–wave by 8%(7.8±0.4 vs 8.5±0.4 ms, p=0.011) compared to contralateral BSS treated eyes. Similarly, oscillatory potentials (OP)implicit times were shortened for OP2 (4.7%, p=0.047), OP3 (4.3%, p=0.023), and OP4 (4.0%, p=0.03) versus BSS control. Signal amplitudes were not significantly affected, however, increases were observed for OP3 (20%) and OP4 (38%)amplitudes.

Conclusions: : CA–I induces retinal leukocyte adhesion after 48 hours. The effect is blocked by acetazolamide indicating a possible role for Ca and retinal inflammation. Changes in electrophysiology suggest that Ca–I may effect ocular acid base regulation and alter neuronal polarization.

Keywords: retina • electroretinography: non-clinical • imaging/image analysis: non-clinical 
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