Speaker
Description
Glaucoma is a leading cause of blindness worldwide that is characterized by irreversible vision loss. In addition to elevated intraocular pressure (IOP), impairments in retinal blood flow and oxygenation have been shown to contribute to the progression of glaucoma. We extend our existing model of the retinal vasculature, which includes blood flow and oxygen transport mechanisms, to incorporate venous collapsibility. Venules are modeled as Starling resistors, allowing collapse when external pressure exceeds intravascular pressure. Retinal blood flow and tissue oxygenation are predicted as intraluminal pressure and IOP are varied. At baseline IOP, blood flow remains relatively constant across a physiological pressure range (autoregulation plateau). Elevated IOP shifts this plateau to higher pressures, reducing autoregulatory capacity. At elevated IOP, the oxygen extraction fraction decreases sharply as arterial pressure increases. This suggests that venous collapse alters microvascular flow distribution and limits effective oxygen utilization despite increased perfusion pressure. Ultimately, the inclusion of venous collapsibility in the model yields more accurate predictions of the impact of IOP on autoregulation and hemodynamic dysfunction in glaucoma. This model framework will allow for future comparisons to sectorial-specific clinical data to assess the role of impaired blood flow regulation in ocular disease.
Bibliography
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volume = {66},
copyright = {http://creativecommons.org/licenses/by-nc-nd/4.0/},
issn = {1552-5783},
url = {https://iovs.arvojournals.org/article.aspx?articleid=2802485},
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language = {en},
number = {1},
urldate = {2026-03-24},
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pages = {42},
}
