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Abstract
Five pairs of excised human eyes were examined for anatomic correlates of changes in aqueous outflow facility that result from changing the intraocular pressure (IOP) and from placing mechanical tension on the irido-corneal angle (lens depression). An increase in IOP from 0 to 40 mm Hg tended inconsistently to compress trabecular meshwork as a whole and to distend the juxtacanalicular tissue. The most constant and significant effect of increasing IOP, however, was to compress Schlemm's canal, thereby progressively diminishing its volume to its virtual collapse at 40 mm Hg IOP. Lens depression increased Schlemm's canal volume and partially prevented its collapse at high levels of IOP. The mean frequency of endothelial vacuoles was remarkably constant at IOPs from 2.5 to 40.0 mm Hg, with and without lens depression, but was significantly lower when the IOP was reduced to 0 mm Hg. When correlated with existing physiologic data, these anatomic findings suggest that Schlemm's canal collapse, but not vacuole frequency, is an important contributor to pressure-dependent changes in aqueous outflow facility.