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L. M. Wood, F. Tremblay; Characterization of Isoflurane Anesthesia on Retinal Physiology. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5580.
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Previous clinical observation documented the impact of isoflurane anesthesia on the electroretinographic signal (ERG). Here, we examined in vitro the effect of isoflurane anesthetic on the guinea pig retinal physiology.
Guinea pig retinae were dissected and placed ganglion cells (RGCs) down on a 8 x 8 microelectrode array (30 µm electrodes diameter, 500µm spacing). Long-duration light stimuli (LED 530nm, 500ms, 10-50 cd•m-2 ) were used to generate ERG as well as RGC action potentials. Post-stimulus time histograms were generated by windowing RGC spiking activity and ERGs were averaged out. Counts were made of spontaneous activity, as well as responses associated with ON and OFF stimuli, while ERG amplitude and implicit times were measured. After baseline recordings, the retina was superfused with various dilutions of Ames media at 37°C saturated with isoflurane.
ERG data cumulated in patients under isoflurane anesthesia disclosed alteration of the OFF component.1 Retrobulbar ERG recordings from a swine model revealed that all evoked potentials related to optic nerve activity were significantly attenuated after isoflurane anesthesia.2 Our in vitro assay documented an isoflurane dose-related loss of RGC spontaneous spiking activity. The OFF responses to long-duration stimuli appear to be more sensitive than the ON responses. At high concentration corresponding approximately to 3 MAC, all spiking activity disappeared, in keeping with a proposed action on voltage-gated sodium channels (Nav); however the ERG a-wave was also significantly reduced, suggesting additional mechanisms. The effects were fully recoverable.
Isoflurane anesthesia exerts a profound influence on retinal processing as quantified by ERG and RGCs activity. Recognition of those effects at the retinal level is essential for appropriate interpretation of in vivo recordings and is particularly important to decipher the cortical responses evoked in animal models.1 Tremblay F & Parkinson J. (2003). Doc Ophthalmol. 107:271-2792 Lalonde MR, Chauhan BC, Tremblay F. (2002). Invest Ophthal Vis Sci. 43: E-abstract 1819
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