Neuroprotective Effect of Hyperbaric Oxygen Therapy on Anterior Ischemic Optic Neuropathy

Abstract

The study investigated the therapeutic effect of hyperbaric oxygen (HBO) on anterior ischemic optic neuropathy in a rodent model (rAION). rAION was laser-induced in one eye of 63 mice. The fellow (uninjured) eye served as an internal control. Thirty-three mice underwent two 90-min sessions of 100% oxygen (2 atm) treatment immediately following injury and one session daily thereafter for up to 14 days. The remaining mice were untreated. Retinas were harvested at different time points, and mRNA levels of various genes were analyzed by real-time polymerase chain reaction and histologic study. Untreated mice: day 1 post-rAION – SOD-1 (oxidative-stress-related) decreased to 82% of control (uninjured eye) levels (P < 0.05), Caspase-3 (proapoptotic) decreased to 89%, Bcl-xL mildly increased (117%; all NS); day 3 – HO-1 and endothelial nitric oxide synthase (eNOS; ischaemia-related) decreased to 74%, and Bcl-2-associated X protein, Caspase-3, and B-cell lymphoma 2 (Bcl-2; apoptotic) increased by 170, 120, and 111%, respectively (all NS); day 21 – HO-1 increased to 222% (NS) and eNOS decreased to 48% (P < 0.05). Treated mice: day 1 – SOD-1 and Caspase-3 remained unchanged, Bcl-2 and Bcl-xL mildly increased (112 and 126% respectively); day 3 – HO-1 and eNOS increased, apoptosis-related gene decreased; day 21 – SOD-1 decreased whereas eNOS increased (P < 0.05), and HO-1 increased to a lesser degree than without treatment. None of the oxygen-treated animals had retinal ganglion cell loss or a decrease in Thy-1 expression. In conclusion, HBO treatment after rAION induction influences the expression of apoptosis-related genes as well as oxidative-stress-induced and ischaemia-related genes and may exert a neuroprotective effect.

Relative neuroprotective effects hyperbaric oxygen treatment and TLR4 knockout in a mouse model of temporary middle cerebral artery occlusion

“…After removal of the filament and wound closure, animals receiving HBOT were placed in a chamber containing 100% oxygen at 2.5 atmospheres pressure for 60 minutes, as previously reported [11], without receiving further anesthesia. The time between filament removal and achieving 2.5 atmospheres 100% oxygen was approximately 10 minutes.…”

Hyperbaric oxygen pre‐treatment impairs anoxic tolerance but improves hyperglycemic tolerance in peripheral nerve

“…[9][10][11][12][13][14][15] In addition, there have been a number of studies searching for the effect of hyperbaric oxygen on radiation induced optic neuropathy 16,17 and ischemic optic neuropathy. 18,19 Kihara 20 showed a positive effect to of HBO on experimental ischemic neuropathy. Only a few studies have addressed the effect of hyperbaric oxygen on other types of neuropathy.…”

“…There is evidence from multiple investigators to support a positive effect of HBO in accelerating recovery after traumatic nerve injury . In addition, there have been a number of studies searching for the effect of hyperbaric oxygen on radiation induced optic neuropathy and ischemic optic neuropathy . Kihara showed a positive effect to of HBO on experimental ischemic neuropathy.…”

Translational Preclinical Research may Lead to Improved Medical Management of Non-Arteritic Anterior Ischemic Optic Neuropathy

“…Rodent models of AION (rAION) have so far proved invaluable for testing potential novel treatments. Hyperbaric oxygen administered during the critical period immediately after induction of injury proved effective in preventing RGC loss ( 50 ). Intravenous or intravitreous prostaglandin J2 proffered almost equal protection when administered 5 h before rAION injury or immediately after, suggesting that it may have an even longer therapeutic window in humans in whom the injury develops more slowly, with episodes of recurring ONH edema ( 51 , 52 ).…”