Abstract
Purpose: :
To assess the rigidity of ageing human Bruch’s from the macular region of the fundus and evaluate the effect of this parameter on the transport dynamics of the membrane
Methods: :
Isolated samples of Bruch’s–choroid were mounted in specialized open horizontal Ussing–type chambers such that the exposed curvature of Bruch’s membrane could be tracked by OCT. Hydrostatic pressures (range 5–30 mmHg) were applied from underneath and corresponding changes in membrane topography recorded. The resulting image analysis allowed calculation of arc–length subtended by Bruch’s in response to the applied pressure. Change in arc–length per unit applied pressure provided the elasticity index and degree of membrane rigidity. The analysis also provided a measure of the exposed surface area at each given pressure. Transport function was determined employing the same pressure range to induce fluid flow and recorded as hydraulic conductivity of the membrane. Membrane thickness was determined from histological sections. Altogether, 35 samples were examined in the donor age range13–90 years.
Results: :
In macular regions, the rigidity of Bruch’s membrane, expressed as the elastic index, ranged from 3.0 X 10–4 in the 13 year old to 0.6 X 10–4 mm/Pa in the 90 year old donor, the age–dependent decrease being linear with correlation coefficient r = –0.97 and significance p< 0.001. Similar changes were observed in the peripheral fundus, r = –0.54 and p< 0.001. Transport function, as assessed by hydraulic conductivity, showed an exponential decline with age from 8.38 X 10–11 m/sec/Pa in the 13 year old to 0.31 X 10–11 m/sec/Pa in the 90 year old sample, the declining age relationship being significant with p< 0.001. A cross correlation demonstrated that decreasing elasticity of Bruch’s was associated with an exponential decline in hydarulic conductivity of the membrane.
Conclusions: :
Bruch’s rigidity may be pivotal in maintaining patent pathways for fluid and nutritional transport across the membrane and its demise with age may therefore contribute to the pathogenesis of age–related macular degeneration.
Keywords: age-related macular degeneration • Bruch's membrane • retinal degenerations: cell biology