Prolonged and intermittent normobaric hyperoxia induce different degrees of ischemic tolerance in rat brain tissue

Effects of hyperoxia exposure on metabolic markers and gene expression in 3T3-L1 adipocytes

“…Moreover, some animal studies have demonstrated that treatment with hyperoxia might produce beneficial effects in different metabolic disorders, such as protecting the rat brain tissue against ischemia reperfusion injury [5], reducing severity of colitis [11] or ameliorating hemorrhagic shock-induced renal failure by decreasing intrarenal hypoxia and improving renal functions [10]. Additionally, several studies have shown that hyperoxia can decrease the expression of some pro-inflammatory genes in different organs and cell types.…”

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

“…To our knowledge, besides the few hyperoxic preconditioning investigations performed on rat and mice hearts [10,20] and rat and rabbit central nervous systems, [4,21] there is only one study reported in 2008 about the effect of hyperoxic exposure on inducing rat renal ischemic tolerance. [22] It is not clear in this study that the protective effects of 1 h/day hyperoxic pretreatment for five days are purely due to the late effects of oxygen pretreatment, as the rats were subjected to only in the last day of oxygen exposure.…”

“…Different stimuli can induce ischemic tolerance, like ischemia itself, heat stress, hypoxia, and oxidative stress. [4,5] Ischemic preconditioning is a potent mode of organ 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.…”

“…[4,5] Ischemic preconditioning is a potent mode of organ 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.…”

“…[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. [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.…”