Abstract
ObjectivesTo explore the effect of ketamine-xylazine anesthesia on light-induced retinal degeneration in rats.MethodsRats were anesthetized with ketamine and xylazine (100 and 5 mg, respectively) for 1 h, followed by a recovery phase of 2 h before exposure to 16,000 lux of environmental illumination for 2 h. Functional assessment by electroretinography (ERG) and morphological assessment by in vivo imaging (optical coherence tomography), histology (hematoxylin/eosin staining, TUNEL assay) and immunohistochemistry (GFAP and rhodopsin staining) were performed at baseline (ERG), 36 h, 7 d and 14 d post-treatment. Non-anesthetized animals treated with light damage served as controls.ResultsKetamine-xylazine pre-treatment preserved retinal function and protected against light-induced retinal degeneration. In vivo retinal imaging demonstrated a significant increase of outer nuclear layer (ONL) thickness in the non-anesthetized group at 36 h (p<0.01) and significant reduction one week (p<0.01) after light damage. In contrast, ketamine-xylazine pre-treated animals showed no significant alteration of total retinal or ONL thickness at either time point (p>0.05), indicating a stabilizing and/or protective effect with regard to phototoxicity. Histology confirmed light-induced photoreceptor cell death and Müller cells gliosis in non-anesthetized rats, especially in the superior hemiretina, while ketamine-xylazine treated rats showed reduced photoreceptor cell death (TUNEL staining: p<0.001 after 7 d), thicker ONL and longer IS/OS. Fourteen days after light damage, a reduction of standard flash induced a-wave amplitudes and a-wave slopes (p = 0.01) and significant alterations in parameters of the scotopic sensitivity function (e.g. Vmax of the Naka Rushton fit p = 0.03) were observed in non-treated vs. ketamine-xylazine treated animals.ConclusionsOur results suggest that pre-treatment with ketamine-xylazine anesthesia protects retinas against light damage, reducing photoreceptor cell death. These data support the notion that anesthesia with ketamine-xylazine provides neuroprotective effects in light-induced cell damage.
Highlights
The term neuroprotection refers to an intervention that may prevent, retard or reverse neuronal cell death after acute or during chronic insult [1]
Evidence of the neuroprotective effect of anesthetics includes the capacity of general anesthesia to increase neuronal tolerance to hypoxic and ischemic insults [3,4] and their protective effects in neurodegenerative diseases [5] including Alzheimer [6] and animal models of Parkinson [7]
In axotomized rat retinal ganglion cells (RGC) neuroprotection has been reported in vivo when combinations of chloral hydratebuprenorphine, ketamine-xylazine or fentanyl-medetomidine-midazolam were used for anesthesia; chloral hydrate alone or in combination with carprofen did not affect the numbers of surviving RGCs [8]
Summary
The term neuroprotection refers to an intervention that may prevent, retard or reverse neuronal cell death after acute or during chronic insult [1]. Evidence of the neuroprotective effect of anesthetics includes the capacity of general anesthesia to increase neuronal tolerance to hypoxic and ischemic insults [3,4] and their protective effects in neurodegenerative diseases [5] including Alzheimer [6] and animal models of Parkinson [7]. The ability of light to cause severe retinal degeneration has been well described [9,10]. Retinal light damage is used as model for human retinal degeneration (RD) arising from environmental insult, aging and genetic disease [11]. We used a very similar protocol as described by Grimm et al to induce profound retinal degeneration [12]
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