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Editors Selection IGR 10-2

Basic research: Investigative neuroprotection

Comment by George Cioffi on:

11773 Amelioration of endothelin-1-induced optic nerve head ischemia by topical bunazosin, Goto W; Oku H; Okuno T et al., Current Eye Research, 2005; 30: 81-91

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The study by Goto et al. (295) presents an extensive set of experiments in which endothelin-1 injections into the vitreous cavity were used to produce an ischemic optic neuropathy with documented retinal ganglion cell loss and optic nerve cupping in a rabbit model. The authors then conducted a formal set of comparison experiments using topical bunazosin (an 1-adrenergic antagonist) in an attempt to block the effects of endothelin-1. The authors measured optic nerve blood flow with a laser speckle technique and also monitored optic nerve structure, as well as function (visual evoked potentials, VEP). While the repeated injections of endothelin-1 decreased optic nerve blood flow, prolonged the VEP implicit time, and caused a loss of retinal ganglion cells with associated cup enlargement, the topical bunazosin appeared to block all these effects. Interestingly, very little change in intraocular pressure (IOP) was seen with any of the treatment groups. This demonstrates that elevated IOP is not a prerequisite for cupping. The authors were careful to perform both vehicle-controlled studies against the topical administration of bunazosin, as well as sham injection experiments in place of the endothelin-1 intravitreal injections.

Bunazosin appears to protect theretina and optic nerve against the ischemic effect of endothelin-1

The data is intriguing, both because of its findings in the chronic endothelin-1 animals in which optic nerve cupping and functional loss was detected associated with a purely ischemic insult. As well, this -adrenergic blocker when administered topically appears to protect the retina and optic nerve against the ischemic effects of endothelin-1. The authors note that the vascular architecture of the rabbit optic nerve is quite similar to humans. This is especially on the arterial side of the equation, but the venous side is quite different. As well, the retinal and optic nerve architecture is quite dissimilar from the primate eye (including humans), the author's findings, coupled with the apparent cupping of the optic nerve, forces us to re-examine our concept of elevated intraocular pressure being required for optic nerve cupping. In fact, cupping is seen in this animal despite its lack of a true lamina cribrosa. Expansion of such experiments in higher animals (possibly even primates) would be of great interest. The authors should be congratulated for their well described and thought out experiments and I look forward to further protocols employing topical bunazosin.

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