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Vinicius Vanzan Pimentel Oliveira, Adalmir M Dantas, Marcio M Rodrigues; PRESSURE TRIGGERS RETINAL SPREADING DEPRESSION AND ITS BLOCKAGE BY BRIMONIDINE TATRATE. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1885.
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© ARVO (1962-2015); The Authors (2016-present)
Spread depression (SD) was originally on retina by Gouras (1958). SD is widely associated with neuronal damage. While it spreads through retina, electrical and intrinsic optical signs can be measured. The main purposes of this paper are: (1) demonstrate if hydrostatic pressure can trigger SD and (2) to identify if brimonidine tartarate (BT) is able to reduce, block, or even do not let start the spreading phenomena.
We performed 25 experiments on fragments of retinal preparations of White Leghorn chicks from 3 to 8 days after hatching. Immediately after decapitation the eyeballs were removed and sectioned along the equator. Fragments of retina were transferred to a closed chamber and infused with modified Ringer solution (RS) driven by a peristaltic pump in order to maintain the RS flowing at a rate from 0.8 to 0.85 ml/min. The presence or absence of SD was detected by recording its concomitant slow voltage variations. The retina was infused with RS and the pressure inside the chamber was kept at atmospheric pressure. After 15 minutes pressure was raised to 20 mmHg. Then after 15 min another increase of 20 mmHg was made, at a total of 40 mmHg. The same protocol was repeated with fresh retinal tissue infusing RS + BT at 0.2%. Graphs and statistical analysis were made with GraphPad Prism 5.03, using t-test of Student.
Our results demonstrate that pressure is capable of trigger SD. There was no significant difference between SD voltage elicited by 20 or 40 mmHg. We also observed that BT was able to prevent SD.
SD has been associated to many central nervous disorders as stroke, intracranial hypertension and trauma. On this context, to evaluate if retina is susceptible to the same kind of injury permits novel kind of understanding of the phenomenon. As it occurs on glaucoma, high pressure applied to retinal tissue damage it as it can trigger SD (a lesion wave). Although the main BT pathway action is still not well known, it is clear its powerful effect. The recent association of SD with many traumatic disorders of the central nervous tissue leads us to wonder how BT blocks SD, possibly acting as a neuroprotector drug. Its possible acting pathway a Gi-protein mediated response, down regulating AMPc is a strong possibility. Further studies are necessary trying to explain the pathophysiology of the experiment.
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