Blood-retinal barrier breakdown following experimental retinal ischemia and reperfusion

The purpose of this study was to examine the effects of acute ischemia and reperfusion on blood-retinal barrier (BRB) function in the rabbit eye. Hydrostatic pressure (140 mmHg) was used to create total retinal ischemia for intervals of 20, 40, 60, 80 or 100 min in the rabbit eye. The location, size...

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Veröffentlicht in:Experimental eye research 1995-11, Vol.61 (5), p.547-557
Hauptverfasser: Wilson, Charles A., Berkowitz, Bruce A., Funatsu, Hideharu, Metrikin, David C., Harrison, David W., Lam, Michael K., Sonkin, Peter L.
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Sprache:eng
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Zusammenfassung:The purpose of this study was to examine the effects of acute ischemia and reperfusion on blood-retinal barrier (BRB) function in the rabbit eye. Hydrostatic pressure (140 mmHg) was used to create total retinal ischemia for intervals of 20, 40, 60, 80 or 100 min in the rabbit eye. The location, size and permeability-surface-area product normalized to the area of retinal leakage (PS') of ischemia-induced BRB lesions were then measured using contrast-enhanced magnetic resonance imaging (MRI) after various intervals of reperfusion. Diffuse outer BRB leakage occurred in most eyes subjected to 80 or 100 min of ischemia. A posterior region of outer BRB sparing was found in eyes that underwent lesser durations of ischemia. On day 1 after retinal ischemia, a linear relationship was found between mean PS' and duration of ischemia for periods of ischemia between 20 and 100 min [slope: 5·65 × 10 −6 to 5·96 × 10 −6 cm min −1 (min ischemia) −1; r 2 ⩾ 0·69]. Lesion size also increased between 20 and 100 min of ischemia. In a longitudinal study, eyes exposed to 60 min of ischemia showed a decrease in PS' and a lesion size over an 8-week period of observation. However, leakage was still present on post-ischemia day 57 in two of three eyes examined. Data obtained in these experiments are expected to prove useful in future studies aimed at understanding how BRB damage relates to neuroretinal damage after ischemia-reperfusion injury.
ISSN:0014-4835
1096-0007
DOI:10.1016/S0014-4835(05)80048-X