Effect of sevoflurane preconditioning on light-induced retinal damage in diabetic rats.

Hyperglycemia and bright light are powerful stress agents that produce an enhanced retinal damage, when simultaneously acting on retina. Previous studies have shown that preconditioning with sevoflurane anesthesia offers a certain degree of protection to retinal cells against light damage. The objective of this study was to explore the effect of sevoflurane anesthetic preconditioning on a model of light-induced retinal degeneration in diabetic rats. Wistar rats that were randomly divided into four groups: control (rats exposed to photostress), group 1 (rats exposed to photostress and sevoflurane preconditioning), group 2 (diabetic rats exposed to photostress), group 3 (diabetic rats exposed to photostress and sevoflurane preconditioning) were used for this experiment. We recorded basal electroretinogram (ERG), at 36 h and 14 days after photostress and performed histological analysis of the retina. Results showed that sevoflurane has a protective effect on light-induced neuroretinal degeneration proved by significantly less variations of the ERG before and after photostress. Diabetes appears to increase the damaging effect of photostress on retina and attenuate the protection provided by sevoflurane preconditioning.

Electrophysiologic evaluation of the visual pathway at different depths of sevoflurane anesthesia in diabetic rats.

Our study investigated the changes produced by diabetes on the visual pathway in a Wistar rat model. The impact of diabetes at 10 weeks after intraperitoneal streptozotocin (STZ) injection was evaluated through electrophysiological methods like visual evoked potentials (VEP) and electroretinogram (ERG). VEP and ERG were recorded simultaneously under different sevoflurane anesthetic depths. In all tested concentrations, sevoflurane affected the amplitude and latency of VEP and ERG component elements. With increasing anesthetic depths, sevoflurane increased the latencies of VEP N1, P1 and N2 peaks and ERG a- and b- waves in both control and diabetic animals. On the other hand, the amplitude of VEP showed enhancement in higher concentrations of sevoflurane, contrariwise to the drop of amplitude seen in the ERG. Diabetes additionally increased the latencies of VEP peaks and decreased the N1-P1 amplitude of the VEP when compared to control at the same anesthetic depth. The a- and b- waves were also delayed by diabetes at 10 weeks post-STZ diabetic induction, with the exception of highly profound anesthetic depth in which the result for the b wave were conflicting. We found a reduction in amplitude of the a-b wave in diabetic animals, when ERG was recorded under 6% and 8% sevoflurane concentration. In conclusion, neurophysiological studies like VEP and ERG are useful in the assessment of retinal and optic nerve dysfunctions produced by diabetes, yet considering the alterations that occur during anesthesia if this is used.