Structural and Functional Imaging of the Retina in Central Retinal Artery Occlusion - Current Approaches and Future Directions.

Central retinal artery occlusion (CRAO) is a form of acute ischemic stroke which affects the retina. Intravenous thrombolysis is emerging as a compelling therapeutic approach. However, it is not known which patients may benefit from this therapy because there are no imaging modalities that adequately distinguish viable retina from irreversibly infarcted retina. The inner retina receives arterial supply from the central retinal artery and there is robust collateralization between this circulation and the outer retinal circulation, provided by the posterior ciliary circulation. Fundus photography can show canonical changes associated with CRAO including a cherry-red spot, arteriolar boxcarring and retinal pallor. Fluorescein angiography provides 2-dimensional imaging of the retinal circulation and can distinguish a complete from a partial CRAO as well as central versus peripheral retinal non-perfusion. Transorbital ultrasonography may assay flow through the central retinal artery and is useful in the exclusion of other orbital pathology that can mimic CRAO. Optical coherence tomography provides structural information on the different layers of the retina and exploratory work has described its utility in determining the time since onset of ischemia. Two experimental techniques are discussed. 1) Retinal functional imaging permits generation of capillary perfusion maps and can assay retinal oxygenation and blood flow velocity. 2) Photoacoustic imaging combines the principles of optical excitation and ultrasonic detection and - in animal studies - has been used to determine the retinal oxygen metabolic rate. Future techniques to determine retinal viability in clinical practice will require rapid, easily used, and reproducible methods that can be deployed in the emergency setting.

Staurosporine-induced differentiation of the RGC-5 cell line leads to apoptosis and cell death at the lowest differentiating concentration.

BACKGROUND: Supplementation of staurosporine is the method of choice for differentiating the solely existing retinal ganglion cell (RGC)-5 cell line. This differentiation was initially claimed to be in the absence of apoptosis, but some publications supposed the induction of apoptosis during staurosporine induced RGC-5 differentiation. In respect to these inconsistencies in the literature, we investigated in detail whether RGC-5 cell differentiation by staurosporine induces apoptosis or not. METHODS: Amounts of 50 nM, 200 nM, 300 nM, and 600 nM of staurosporine were supplemented on RGC-5 cells for 24 h. Cell morphology and cell death, via propidium iodide staining, were evaluated with phase contrast and fluorescence microscopy, respectively. Cell amount, cell proliferation, and cell viability were analyzed by crystal violet staining, CFSE flow cytometry, and MTS assay, respectively. Apoptosis was determined by analyzing caspase 3/7 activity, Annexin-V+/ 7AAD- cells and the quotient of Bax to Bcl-2 mRNA expression via caspase 3/7 activity assay, flow cytometry, and real-time PCR, respectively. RESULTS: RGC-5 cells started to change their morphology and their expression of neuronal markers at 50 nM of staurosporine. This was associated with apoptosis and cell death, as indicated by a 2.1-fold (p < 0.0005) increase in caspase 3/7 activity, a 1.2-fold (p < 0.05) induction of Annexin-V+/ 7AAD- cells, and a 12-fold (p < 0.0005) increase in propidium iodide positive cells, respectively. Furthermore, staurosporine led to a dose-dependent increase in apoptosis and reduction in cell viability, cell density, and cell proliferation. CONCLUSIONS: The lowest staurosporine concentration inducing RGC-5 cell differentiation is accompanied by apoptosis and cell death.

Fluctuations of the Intraocular Pressure in One Eye Influence the Intraocular Pressure in the Fellow Eye.

PURPOSE: To investigate the ophthalmotonic consensual reaction (OCR) in healthy individuals. METHODS: This was a cohort study of 59 pairs of eyes of patients who underwent cataract surgery in one eye and had no other ocular pathology than cataract. Main outcome measure was change of intraocular pressure (IOP) in the untreated fellow eye. The IOP was measured 1 hour before, 1 hour after, and 1 day after surgery. RESULTS: One hour after surgery, IOP decreased in 24 (41%) operated eyes (group A). In the corresponding untreated fellow eyes (group Af), the mean IOP (±standard deviation [SD]) did not change (14.1 ± 3.0 mmHg preoperatively to 14.2 ± 3.1 mmHg postoperatively, p = 0.8). Only two operated eyes showed unchanged IOP (group B). In 33 (56%) operated eyes, the IOP increased (group C). In the untreated fellow eyes (group Cf), the mean IOP decreased significantly from 15.1 ± 2.9 to 13.7 ± 2.6 mmHg (p = 0.0012). One day after surgery, the mean IOP of group Af decreased significantly from 14.2 ± 3.1 (postoperative IOP) to 12.7 ± 3.2 mmHg (p = 0.007). In group Cf, the mean IOP revealed no changes from 13.7 ± 2.6 to 13.5 ± 2.4 mmHg (p = 0.69). CONCLUSIONS: Our results showed some evidence for the existence of the OCR in healthy individuals. Significant IOP elevation in one eye resulted in IOP reduction in the fellow eye. Interestingly, this phenomenon did not exist vice versa.