May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Increased Corneal and Anterior Chamber Inflammatory Response after an Alkali Burn during Hyperlipidemia
Author Affiliations & Notes
  • M.D. Anton
    Opthalmology, Risquez Hospital, Caracas, Venezuela
  • A. Behrens
    Opthalmology, Risquez Hospital, Caracas, Venezuela
  • B.E. Brito
    Experimental Medicine, Venezuelan Institute for Scientific Research (IVIC), Caracas, Venezuela
  • Footnotes
    Commercial Relationships  M.D.V. Anton, None; A. Behrens, None; B.E. Brito, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1386. doi:
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      M.D. Anton, A. Behrens, B.E. Brito; Increased Corneal and Anterior Chamber Inflammatory Response after an Alkali Burn during Hyperlipidemia . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1386.

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

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Abstract

Abstract: : Purpose: To determine if a hyperlipidemic diet increases the ocular inflammatory response in a corneal alkali burn model in rabbits. Methods: New Zealand White rabbits (3.5-4 Kg) were fed with one of the following diets during 8 weeks: a) Hypercholesterolemic diet: 0.3% cholesterol dissolved in corn oil for the first 4 weeks and 0.1% cholesterol for the last 4 weeks (HChR, n=6), b) Corn oil diet: Chow impregnated with corn oil (CR, n=6), and c) Normal diet (NR, n=6). At the end of the treatment a corneal chemical burn was produced with the application of a 2 mm disc soaked in 1 N NaOH for 40 sec. A saline soaked disc was applied in the contralateral eye as control. Aqueous humor (AH) was harvested 8 h after the burn and the number of infiltrating cells were determined. Total protein in AH was measured by a colorimetric assay and IL-6 activity by B9 bioassay. Corneas were fixed and embedded in paraffin. Corneal limbal infiltrating cells were determined in 5 µm sections stained with H & E. Cholesterol and triglycerides levels were measured by colorimetric assay. Results are expressed as mean±SE. Results: Alkali burn of corneal surface induced the infiltration of cells into AH. CR cells (7.1±0.2×105 cells/ml) were significantly increased (p=0.04) compared to NR (2.4±0.2×105 cells/ml), while no significance (p=0.3) was found between HChR (6.9±0.5×105 cells/ml) and their saline controls (p=0.03). Total proteins were only significantly increased (p=0.02) in HChR (29.8±5.7 mg/ml) compared to NR (17.2±8.8 mg/ml). No significant difference was found on IL-6 levels between HChR (1556±277.3 pg/ml), NR (1956.9±584.9 pg/ml) and CR (14763.2±13540.4 pg/ml). After the chemical burn, all of the 6 corneas of NR showed a moderated limbal infiltration (210.2±9.03 cells), while a stronger and significant cell infiltration was observed in HChR (288.2±8.3 cells, p=0.03) and CR (405.2±18.3 cells, p=0.004). Cholesterol levels in HChR (594.6±72.8 mg/dl) were significantly (p=0.03) increased vs NR (73.6±20.1 mg/dl). Conclusions: To our knowledg, this is the first report showing that hyperlipidemic diets induce an increased inflammatory limbal corneal response after an alkali burn, being this cell infiltration higher in CR followed by HChR and NR. This injury also influenced the anterior chamber inflammatory response being similar in CR and HChR compared to NR. These results also suggests that hyperlipidemia, as for EIU (Brito et al. ARVO Meeting 2001), might play a role in the increase of susceptibility to other ocular inflammatory processes.

Keywords: inflammation • cornea: basic science • lipids 
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