Purchase this article with an account.
Lucia Carichino, Alon Harris, Giovanna Guidoboni, Brent A Siesky, Luis Pinto, Evelien Vandewalle, Olof Birna Olafsdottir, Ingeborg Stalmans, Einar Stefansson, Julia Concetta Arciero; A theoretical investigation of the increase in venous oxygen saturation levels in glaucoma patients. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2739.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Several clinical studies (e.g. Olafsdottir and Vanderwalle et al. 2014) have observed increased retinal venous oxygen (O2) saturation in glaucoma patients as compared with healthy persons (Fig. 1A). Here, a theoretical model is used to propose three possible explanations for these observed increases in saturation.
A previously developed theoretical model of the retina (Arciero et al. 2013) is used to predict changes in blood flow and O2 saturation in retinal arterioles, capillaries, and venules. Tissue O2 consumption is calculated using a Krogh cylinder model. Given clinical measurements of intraocular pressure (IOP), mean arterial pressure (MAP), and arterial O2 saturation from healthy persons and advanced (visual field MD≥10dB) primary open angle glaucoma (POAG, IOP>21mmHg) and normal tension glaucoma (NTG, IOP≤21mmHg) patients, the model is used to predict the O2 demand (M0) or capillary density (N) that would yield the clinically-measured venous O2 saturation in each population.
The model predicts that a decrease in M0, an impairment of autoregulation (IA), or an increase in N can individually lead to increased venous saturation for certain ocular perfusion pressures (OPP=2/3 MAP - IOP), as depicted in Fig. 1B. The model also predicts that a decrease in M0 or increase in N yields increased venous saturation in POAG patients, while no change in M0 or N is predicted in NTG patients when compared with healthy persons.
Decreased M0, impaired regulation, and increased N can independently lead to increased venous saturation, although to different degrees depending on an individual’s OPP level. The study also suggests that the mechanisms leading to increased venous saturation in advanced cases of glaucoma differ between POAG and NTG patients. We hypothesize that the increased saturation levels are explained by decreased M0 in POAG and IA in NTG patients.
This PDF is available to Subscribers Only