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Editors Selection IGR 22-2
Blood Flow: Oxygen saturation and VF damage
Comment by Makoto Araie on:
47975 Retinal oximetry in primary open-angle glaucoma, Olafsdottir OB; Hardarson SH; Gottfredsdottir MS et al., Investigative ophthalmology & visual science, 2011; 52: 6409-6413
The retinal artery is a typical example of an end (terminal) artery which is the only supply of oxygenated blood to a portion of tissue, and oxygen saturation in retinal arteries is of particular importance, because its abnormality will directly and instantly affect the metabolism of retinal tissues, that is, seeing function of the eye. Olafsdottir et al. (1901) measured oxygen saturation in the retinal arterioles and venules in primary open-angle glaucoma (POAG) eyes and found that oxygen saturation in the retinal arterioles was stable, being independent of the extent of visual field damage, or retinal ganglion cell (RGC) damage, due to glaucoma, while oxygen saturation in retina venules showed a significant positive correlation to the extent of the damage and the arterio-venous difference in retinal oxygen saturation decreased along with increased visual field damage. The obtained result is compatible with atrophy of retina in POAG, and implies that hypoxic condition is unlikely to be associated with the retinal damage in the POAG eyes currently tested. The intraocular pressure (IOP) of the most of the POAG patients studied by the authors seemed rather well controlled, and thus, it must be noted that their results may not be directly extrapolated to eyes at risks where glaucomatous damages are in progress. Since the difference in oxygen saturation between retinal and venous blood is more directly related with retinal metabolism than blood flow rate through retinal vessels, if the current method of retinal oxymetry established by the authors is applied to patients with known risks for future progression such as those with recurrent optic disc hemorrhage or uncontrolled high IOP, their method may provide important and interesting information on the metabolism of retina before further glaucomatous damages take place. Further, systemic or topical drug effects on the metabolism of retina, it they exist, can be also evaluated in living human eyes using the authors' method. As the authors correctly pointed out, the results of retinal oxymetry should be correlated in future studies not only to the function (psychopysical perimetric data), but also the structure (thicknesses of circum papillary retinal nerve fiber layer, macular ganglion cell or other macular inner retina layers provided by spectral-domain optical coherence tomography). Then, the retinal oxymetry is expected to yield a large quantity of new information which would improve our understanding of retinal metabolism in POAG. The authors are to be commended for reporting a method which will be very useful not only for in-vivo evaluation of retinal pathophysiology in glaucoma, but also for in-vivo pharmacological studies of retina.
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