Título / Title

BRIMONIDINE NEUROPROTECTIVE EFFECT IN PRESSURE RETINAL SPREDING DEPRESSTION

Introdução / Purpose

No drug can be considered a true neuroprotector, acting directly on the neurons, until now. Brimonidine tartrate (BT), an alpha-2 adrenergic drug, is widely used on the treatment of glaucoma and, besides its hypotensive effect on intraocular pressure, a direct neuroprotector effect may be present.
Our early work showed that BT, on chick retina, slowed and even blocked the passage of a wave of neuronal damage called Spreading Depression (SD), as diminished its voltage variation and implicit time. However, we used a traumatic mechanism to induce SD. Is intra-ocular pressure sufficient to start a SD? Can BT block it? How would SD look like under SD-OCT?

Material e Método / Methods

At present work we used a self-made acrylic chamber to the retina lie in while it is continuously perfused with nutrients, and the pressure over the tissue can be raised up to 40mmHg. We also provided a setup where we can measure the voltage on retina tissue during the SD wave w/o brimonidine.

Resultados / Results

Elevated pressure of 40 mmHg was sufficient to generate SD. Brimonidine was effective in slowing down the velocity and the amplitude of the voltage of SD. OCT showed SD is predominantly a phenomenon of the inner plexiform layer.

Discussão e Conclusões / Conclusion

Thus, BT can securely act on neurosensory retina, beside its hypotensive effect on intraocular pressure; it has a neuronal effect, blocking the neuronal damage wave of SD.

Palavras Chave

Brimonidine, neuroprotection, retinal spreading depression