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Renata F. Ramos, W. Daniel Stamer; Effects of Cyclic Intraocular Pressure on Conventional Outflow Facility. Invest. Ophthalmol. Vis. Sci. 2008;49(1):275-281. doi: https://doi.org/10.1167/iovs.07-0863.
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purpose. In vivo, biomechanical stress plays an important role in tissue physiology and pathology, affecting cell and tissue behavior. Even though conventional outflow tissues are constantly exposed to dynamic changes in intraocular pressure, effects of such biomechanical stressors on outflow function have not been analyzed. The purpose of the present study was to determine the effect(s) of ocular pulse on conventional outflow facility in perfused anterior segments.
methods. The anterior segment perfusion model was used to investigate the impact of ocular pulsation on human and porcine outflow facility. To determine tissue viability of human anterior segments, three complementary techniques (postperfusion morphology and cell density of outflow tissues plus central corneal thickness measurements over time of perfusion) were used.
results. A consistent decrease in outflow facility was observed in response to cyclic intraocular pressure in both porcine (−29.96% ± 6.56; P = 0.009) and human (−27.65% ± 8.26; P = 0.010) perfused anterior segments. Viability data showed no significant difference between control and experimental anterior segments, with respect to postperfusion histologic evaluations (P = 0.227) or change in central corneal thickness over time (P = 0.289). In contrast, the cellularity of the trabecular meshwork in experimental (cyclically pulsed) anterior segments (333.86 ± 22.15 nuclei/field of view) was greater than in the control eyes (290.47 ± 17.60, P = 0.05).
conclusions. Decreased outflow facility in cyclically pulsed anterior segments is not a function of cell or tissue damage, but rather is an active response of the conventional outflow tissues to a biomechanical stimulus. In fact, the observation of increased cellularity in tissues exposed to cyclic stress suggests a physiological benefit of mechanical stress to outflow cells in organ culture.
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