Mechanisms of perioperative corneal abrasions: alterations in tear film proteome

Abstract

Perioperative corneal abrasion is an ophthalmic complication commonly found in patients underwent general anesthesia. In this study, correlations between development of corneal injury and proteomic changes in tear film during general anesthesia were examined using an animal (rabbit) model. Being started after 1-h anesthesia, the process of accumulation of pathological changes in the cornea unequivocally led clinically significant abrasions following 3-6 h of the narcosis. The corneal damage was associated with alterations in profiles of major proteins of the tear film. Analysis of the tear proteome pointed to depression of lachrymal glands function, and suggested serotransferrin, serum albumin and annexin A1 as potential tear markers of the complication. The tear film alterations included fast drop of total antioxidant activity and activity of superoxide dismutase, and decrease in interleukin-4 and increase in interleukin-6 content indicating development of oxidative and pro-inflammatory responses. These findings suggest antioxidant and anti-inflammatory therapy as prospective approach for prevention/treatment of perioperative corneal abrasions. The observed anesthesia-induced effects should be considered in any study of ocular surface diseases employing anesthetized animals.

Mitochondria‐Targeted Antioxidant SkQ1 Prevents Anesthesia‐Induced Dry Eye Syndrome

“…To this end, the animals were exposed to general anesthesia for 0.5-6 h and their corneas were subjected to clinical and morphological examination immediately after the narcosis. The results of fluorescein test indicated anesthesia time-dependent accumulation of corneal epithelium injury in accordance with our previous findings [ 39 ]. Statistical analysis revealed that the incidence of the corneal damage rose with the duration of the narcotic sleep reaching 100% of animals after 5-6 h of the anesthesia ( Figure 1(a) ).…”

“…A rabbit model of anesthesia-induced DES developed in our previous studies [ 6 , 39 ] was selected for further trialing of the antioxidant therapy using SkQ1 eye drops. In order to characterize the basic parameters of the model, we determined the incidence of DES symptoms in rabbits depending on the duration of general anesthesia.…”

“…It is widely regarded that DES pathogenesis involves inflammatory component [ 9 , 39 ]. The oxidative stress of the cornea detected in our DES model can induce inflammatory responses of the ocular surface tissues [ 41 ] that may be sensitive to SkQ1 action.…”

“…Considering these limitations, we employed the rabbit model of the disease since these species share many features of ocular anatomy with humans including eyeball size, its internal structure, and optical system as well as biomechanical and biochemical features [ 42 ]. DES was simulated in rabbits by their exposure to general anesthesia [ 6 , 39 , 41 ]. Indeed, anesthetic injections are known to inhibit lacrimal gland innervations and suppress tear production [ 43 ].…”

Improved Effect of a Mitochondria-Targeted Antioxidant on Hydrogen Peroxide-Induced Oxidative Stress in Human Retinal Pigment Epithelium Cells

“…[25]. In other mitochondrial targeting compounds [10,14,31], we observed that pre-treatment with TPP-Niacin signi cantly enhanced the MMP and improved the mitochondrial ultrastructure in a phenotypic analysis by EM, compared to H 2 O 2 alone. Based on these data, we next analyzed gene expressions of mitochondria-related genes, such as OXPHOS subunits, mitochondrial dynamics, and mitochondrial DNA replication and transcription genes.…”