Preconditioning with Hyperbaric Oxygen and Hyperoxia Induces Tolerance against Spinal Cord Ischemia in Rabbits

Abstract

Serial exposure to high oxygen tension induced ischemic tolerance in spinal cord of rabbits. Simple hyperbaricity (2.5 ATA, 21% O2) did not induce ischemic tolerance.

Hyperoxia-Induced Protection against Rat's Renal Ischemic Damage: Relation to Oxygen Exposure Time

“…For example Esmaili et al showed in an in vivo model of rat regional heart ischemia that 120 or 180 minutes of nearly pure oxygen pretreatment could induce delayed heart ischemic tolerance, [23] but our study demonstrates that in kidney, like the central nervous system, [4,7] it takes longer to make tissue tolerant against ischemiareperfusion damage. In 2007, Bigdeli et al induced delayed rat brain ischemic tolerance after 24 h or 6 days of 4 h/day hyperoxia pretreatment, and Dong et al induced delayed rat spinal cord ischemic tolerance after 5 days of 1h/day hyperoxia pretreatment.…”

“…In 2007, Bigdeli et al induced delayed rat brain ischemic tolerance after 24 h or 6 days of 4 h/day hyperoxia pretreatment, and Dong et al induced delayed rat spinal cord ischemic tolerance after 5 days of 1h/day hyperoxia pretreatment. [7] The underlying mechanisms of hyperoxic and hyperbaric preconditioning are not yet fully understood. It seems that subjecting rats to hyperoxia induces the generation of reactive oxygen species (ROS); therefore, a systemic lowgrade oxidative stress is initiated.…”

“…For this reason, safe non-pharmacological stimuli have been sought after, such as hyperoxia, which has been proved to induce tolerance against ischemic damage in rat and mice heart, [9,10] rat brain, [4,11] and rabbit spinal cord. [7] In rat heart, 60 min of hyperoxia (≥ 95% O 2 ), though in rabbit spinal cord 5 days of 60 min/day hyperoxia, could evoke ischemic protection.…”

“…[4,5] It has been suggested that during brief periods of ischemia and reperfusion, trigger substances like nitric oxide, adenosine, and reactive oxygen species (ROS) are released, and signal transduction cascades of protein kinases activate, which induce cell survival programs. [6][7][8][9] Indeed, ischemia and most other stimuli lack potential for clinical use because of associated risks and toxicities. For this reason, safe non-pharmacological stimuli have been sought after, such as hyperoxia, which has been proved to induce tolerance against ischemic damage in rat and mice heart, [9,10] rat brain, [4,11] and rabbit spinal cord.…”

Preconditioning with prolonged oxygen exposure induces ischemic tolerance in the brain via oxygen free radical formation

“…Hyperbaric oxygen (O 2 ) is also able to mimic ischemic preconditioning and induce neuroprotection against ischemic injury in the animal brain and spinal cord. [9][10][11][12][13] It is hyperoxia, not hyperbaricity, that plays the critical role in the induction of tolerance against ischemic injury in the animal brain 11 and spinal cord. 12 Therefore, we hypothesized that the prolonged inhalation of a high concentration of O 2 would result in a similar effect to preconditioning with hyperbaric O 2 .…”