Hyperbaric oxygenation induced tolerance against focal cerebral ischemia in mice is strain dependent

Prass, Konstantin; Wiegand, Frank; Schumann, Pascale; Ahrens, M.; Kapinya, Krisztián; Harms, Christoph; Liao, Weijing; Trendelenburg, George; Gertz, Karen; Moskowitz, Michael A.; Knapp, F.F.; Victorov, Ilya V.; Megow, Dirk; Dirnagl, Ulrich

doi:10.1016/s0006-8993(00)02264-2

Cited by 78 publications

(56 citation statements)

References 18 publications

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“…Significant strain differences in a preconditioning paradigm have been described recently. 7,26 Numerous mediators and mechanisms have been proposed to explain induced ischemic tolerance. Regarding hypoxia as Shown are probes without nuclear extract (lane 1); probes with nuclear extract of a neocortex prepared from a control mouse (lane 2); probes with neocortex prepared immediately after 5 hours of hypoxic preconditioning (5-hour hypoxia; lane 3) and with addition of a specific competitor (lane 4; 50-fold), addition of a nonspecific competitor (lane 5; 50-fold), or addition of a specific antibody against HIF-1␣ (lane 6).…”

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confidence: 99%

Hypoxia-Induced Stroke Tolerance in the Mouse Is Mediated by Erythropoietin

Prass

Scharff

Ruscher

et al. 2003

Stroke

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Background and Purpose-Cellular response to hypoxia is mainly controlled by hypoxia-inducible factor 1 (HIF-1). The HIF-1 target gene erythropoietin (EPO) has been described as neuroprotective. Thus, we hypothesize EPO to be an essential mediator of protection in hypoxic preconditioning. Methods-We randomized Sv129 mice into groups for different pretreatments, different hypoxia-ischemia intervals, or different durations of ischemia. For hypoxic preconditioning, the animals were exposed to a hypoxic gas mixture (8% O 2 and 92% N 2 ) for 30, 60, 180, 300, or 360 minutes. At 0, 24, 48, 72, or 144 hours later, we performed middle cerebral artery occlusion and allowed reperfusion after 30, 45, 60, or 120 minutes, or occlusion was left to be permanent. We studied EPO gene expression in brain tissue with a real-time reverse transcriptase-polymerase chain reaction and measured HIF-1 DNA-binding activity with an electrophoretic mobility shift assay. To block endogenously produced EPO, we instilled soluble EPO receptor into the cerebral ventricle. Results-Hypoxic preconditioning for 180 or 300 minutes induced relative tolerance to transient focal cerebral ischemia, as evidenced by a reduction of infarct volumes to 75% or 54% of the control, respectively. Hypoxic pretreatment was effective only when applied 48 or 72 hours before middle cerebral artery occlusion. Sixty minutes after hypoxia, we found a marked activation of HIF-1 DNA-binding activity and a 7-fold induction of EPO transcription. Infusion of soluble EPO receptor significantly reduced the protective effect of hypoxic pretreatment by 40%. Key Words: erythropoietin Ⅲ ischemic preconditioning Ⅲ stroke Ⅲ transcription factors Ⅲ mice I t has long been known that the brain is very sensitive to hypoxia and ischemia. 1 However, more recently it has been discovered that the brain, like other organs, is capable of inducing protective mechanisms when challenged by stressors or substrate deprivation. 2 These mechanisms, collectively labeled as ischemic tolerance or ischemic preconditioning, are of putative importance for limiting the damage during substrate deprivation. Protection may occur within minutes, 3 but this early tolerant state is lost within hours. However, tolerance can be seen in a second time window after 24 to 48 hours and then lasts for 2 to 3 days. Evidence for the existence of ischemic preconditioning in humans has been reported. 4 The major goal of ischemic preconditioning research at present is to identify the underlying endogenous protective signaling cascades, with the long-term goal to allow therapeutic augmentation of the endogenous protective mechanisms in cerebral ischemia and possibly to induce a protected state of the brain in conditions in which brain ischemia can be anticipated, for example, during surgery of the heart or brain. Conclusions-EndogenouslyTo study the mechanisms of ischemic preconditioning, robust and clinically relevant models are needed. Short and nondamaging periods of focal cerebral ischemia were reported to induce ischemic p...

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confidence: 99%

Hypoxia-Induced Stroke Tolerance in the Mouse Is Mediated by Erythropoietin

Prass

Scharff

Ruscher

et al. 2003

Stroke

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269

208

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“…It has been reported previously that preconditioning with repeated hyperbaric O 2 (HBO) could induce IT in the brain, [9][10][11]13 spinal cord 12 and liver. 18 Wada et al demonstrated that pretreatment with two atmosphere absolute (ATA) HBO once every other day for three or five sessions induced IT in gerbil hippocampus.…”

Section: Methodsmentioning

confidence: 99%

“…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 .…”

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

Zhang

Xiong

et al. 2004

Can J Anesth/J Can Anesth

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“…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.…”

Section: Introductionmentioning

confidence: 99%

“…[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.…”

Section: Introductionmentioning

confidence: 99%