June 2013
Volume 54, Issue 15
ARVO Annual Meeting Abstract  |   June 2013
Author Affiliations & Notes
  • Vinicius Oliveira
    Biophysics Institute, Federal Univ of Rio de Janeiro, Rio de Janeiro, Brazil
  • Renata Fleming
    Biophysics Institute, Federal Univ of Rio de Janeiro, Rio de Janeiro, Brazil
  • Nassim Calixto
    Ophthalmology, Federal Univ of Minas Gerais, Belo Horizonte, Brazil
  • Sebastiao Cronemberger
    Ophthalmology, Federal Univ of Minas Gerais, Belo Horizonte, Brazil
  • Adalmir Dantas
    Biophysics Institute, Federal Univ of Rio de Janeiro, Rio de Janeiro, Brazil
  • Footnotes
    Commercial Relationships Vinicius Oliveira, None; Renata Fleming, None; Nassim Calixto, None; Sebastiao Cronemberger, None; Adalmir Dantas, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 6334. doi:https://doi.org/
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      Vinicius Oliveira, Renata Fleming, Nassim Calixto, Sebastiao Cronemberger, Adalmir Dantas; EFFECTS OF PROPOFOL OVER CIRCULAR RETINAL SPREADING DEPRESSION. Invest. Ophthalmol. Vis. Sci. 2013;54(15):6334. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Spread depression (SD) was first identified 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 circulating spreading depression is a unique model in which once the first stimulus is done, it continuously propagates through the tissue. Propofol is rapidly acting water-insoluble non-barbiturate anesthetic agent that is widely used as an intravenous sedative-hypnotic agent. Recently it was used over cortical SD. The main purpose of this paper is to identify if propofol was able to reduce, or even stop the spreading phenomena.


We performed 30 experiments on retinal of White Leghorn chicks. Retinas were transferred to a chamber and infused with Ringer solution (RS). A circular cut was made in the center of the retina, in order to create a peripheral trail through which the SD circulated. The presence or absence of SD was detected by recording its concomitant slow voltage variations (SVV) through two pore electrodes. The retina was firstly infused with RS and mechanically stimulated by a sharpened tungsten wire, triggering a SD in two opposite directions. MgSO4 blocked one of these branches. After 5 laps, the infusion was changed to RS containing 56.1μM, 224.4μM e 561μM of propofol. Values obtained were divided by the first value observed with RS. Graphs and statistical analysis were made with Graph Pad Prism 6.0, using Bonferroni`s Multiple Comparison Test.


Our data demonstrated that propofol reduces the amplitude of the negative potential shift (SVV graph) - p<0.0001 after 3rd lap with propofol at 56.1μM. SD was blocked with 561μM at first electrode, never getting the second one. Propofol also increased the time interval between two passages through the same electrode (ΔT graph) - p<0.0001 after 2nd lap, and p<0.001 at the 3rd lap.


Propofol acts through GABAa receptor, and, although it reduced the SVV at all concentrations tested, it accelerated the spreading phenomenon at the same concentrations. That acceleration was not observed with local anesthetics (Na channel blockers). Possibly, the SVV reduction through chloride channels elicited the tissue a quick recover from the depolarized stated, which allow SD to move faster through the tissue. At higher doses the neuronal blockage was heavier, which slowed the SD.

Keywords: 690 retina: neurochemistry • 508 electrophysiology: non-clinical  

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