Seminar| Institute of Mathematical Sciences
Time: Wednesday, July 31th, 2024 , 09:00-10:00
Speaker: Lu Yuankai，Univerversity of Pittsburgh
Abstrct: Glaucoma is characterized by progressive degeneration of retina ganglion cells and their axons. The axon damage is believed to start within the lamina cribrosa (LC) region. This can happen at any level of intraocular pressure (IOP) and is likely to worsen if elevated IOP induces LC deformations that distort the vasculature and compromise blood flow. Our goal was to assess the impact of elevated IOP on lamina cribrosa (LC). We hypothesized that elevated IOP would induce both deformation in the LC vasculature and disruption of blood flow within the feeding vessel for LC, i.e., the posterior ciliary arteries (PCA). Since in-vivo LC oxygenation is not yet possible to measure, we used 3D eye-specific numerical models of the LC vasculature, subjected to experimentally-derived deformations and blood flow. We reconstructed detailed 3D models of the ONH vessel networks of 3 healthy monkey eyes using histological techniques. We also obtained in-vivo IOP-induced ONH deformations from a healthy monkey using optical coherence tomography and image tracking techniques while IOP was controlled. A biomechanics-based technique was used to map tissue strains to local vessel distortions. Flow rates within the PCAs were acquired through super-resolution ultrasound techniques in an ex-vivo perfused monkey head, subjected to different IOP conditions. The hemodynamics and oxygenation of the three vessel networks were simulated under deformations from various IOP increases. Both the IOP-induced vessel deformation and reduced PCA flow led to the hypoxia region in LC region. The peripheral vessels have smaller oxygen decreases than the central vessels for various deformations. Our study indicates that different parts of the blood vessels in the ONH have different levels of resistance to elevated IOP. This variation could be linked to the early stages of glaucoma and the subsequent vision loss.