Impact of Elevated Intraocular Pressure on Lamina Cribrosa Oxygenation: A Combined Experimental-Computational Study on Monkeys.

Purpose: To evaluate how lamina cribrosa (LC) oxygenation is affected by tissue distortions resulting from elevated intraocular pressure (IOP). Design: Experimental study on 4 monkeys, histology, and computational analysis. Subjects: Four healthy monkey eyes with OCT scans at IOPs of 10 to 60 mmHg. Methods: Intraocular pressure-induced LC tissue deformations of a healthy monkey were measured in vivo using OCT images and digital volume correlation analysis techniques. Three-dimensional eye-specific models of the LC vasculature of 4 healthy monkey eyes were reconstructed using histology. The models were then used to compute LC oxygenation, first as reconstructed (baseline), and then with the LC vessels distorted according to the OCT-derived deformations. Two biomechanics-based mapping techniques were evaluated: cross-sectional and isotropic. The hemodynamics and oxygenations of the 4 LC vessel networks were evaluated at IOPs up to 60 mmHg to quantify the effects of IOP on LC oxygen supply, assorting the extent of LC tissue mild and severe hypoxia. Main Outcome Measures: Intraocular pressure-induced deformation, vasculature structure, blood supply, and LC oxygenation. Results: Intraocular pressure-induced deformations reduced LC oxygenation significantly and substantially. More than 20% of LC tissue suffered from mild hypoxia when IOP reached 30 mmHg. Extreme IOP (>50 mmHg) led to large severe hypoxia regions (>30%) in the isotropic mapping cases. Conclusions: Our calculations predicted that moderately elevated IOP can lead to mild hypoxia in a substantial part of the LC, which, if sustained chronically, may contribute to neural tissue damage. For extreme IOP elevations, severe hypoxia was predicted, which would likely cause more immediate damage. Our findings suggest that despite the remarkable LC vascular robustness, IOP-induced distortions can potentially contribute to glaucomatous neuropathy. Financial Disclosures: The author(s) have no proprietary or commercial interest in any materials discussed in this article.