Elucidation for pathogenic mechanism of glaucomatous optic neuropathy and retinal ganglion cell death

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As a basic approachWe induced chronically elevated intraocular pressure in rats by injecting India ink into the anterior chamber. One week later, we performed direct laser photocoagulation (PC) of the pigmented band along the corneal limbus directly without using a gonio lens, and injected India ink again to sustain elevated IOP at above 30mmHg for 7 days. We periodically examined the apoptotic changes in the ganglion cells, as well as immunostained caspase-3 in the nerve fiber layer. Apoptotic ganglion cells began to appear on the 3rd day, and became abundant by the 5th day. In contrast, the nerve fiber layer showed a remarkable activation of caspase-3 beginning at 24 hours after IOP elevation and continued thereafter. We clarified the involvement of caspase family in the executive process of the glaucomatous ganglion cell death of the rat acute glaucoma model.As a clinical approachLaser speckle flowgraphy (LSFG) is a non-invasive and quantitative technique that can evaluate intraocular microcirculation. This study included 44 eyes of 44 patients with primary open-angle glaucoma (POAG) and 44 eyes of 44 patients with normal-tension glaucoma (NTG). To evaluate blood flow velocity of optic nerve head, the square blur rate (SBR) was measured by means of LSFG. The correlation between SBR and Humphrey visual field indices was evaluated with linear regression analysis. In the NTG group, SBR was positively correlated with Humphrey visual field indices (r=0.299-0.354, p=0.019-0.049). However, no significant correlation between SBR and Humphrey visual field indices was observed in the POAG group. These results suggested that the change in the circulation of the optic nerve head may be related to visual field damage in the NTG group but may be less involved in visual field damage in the POAG group.