Co-application of ischemic preconditioning and postconditioning provides additive neuroprotection against spinal cord ischemia in rabbits

Jiang, Xiaojing; Shi, Enyi; Liu, Liwen; Nakajima, Yoshiyuki; Sato, Shigehito

doi:10.1016/j.lfs.2007.12.026

Cited by 8 publications

(2 citation statements)

References 30 publications

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“…It has also been shown that the combination of sevoflurane postconditioning, and the acute phase of sevoflurane preconditioning, does not provide greater protection than either alone in rat hearts (Deyhimy et al, 2007). The only study on central nervous tissues showed that the combination of stimuli, which were ineffective when applied alone to induce neuroprotection via the mechanisms of ischemic postconditioning or the acute phase of ischemic preconditioning, significantly improved the neurological functions of rabbits after spinal cord ischemia (Jiang et al, 2008). Our study clearly showed that the combination of isoflurane postconditioning and the delayed phase of isoflurane preconditioning provided greater protection than either alone, suggesting that these two interventions can be combined to further improve the neurological outcomes after a detrimental insult, such as ischemia.…”

Section: Discussionmentioning

confidence: 99%

Isoflurane preconditioning and postconditioning in rat hippocampal neurons

McMurtrey

Zuo

2010

Brain Research

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The volatile anesthetic isoflurane is capable of inducing preconditioning and postconditioning effects in the brain. However, the mechanisms for these neuroprotective effects are not fully understood. Here, we showed that rat hippocampal neuronal cultures exposed to 2% isoflurane for 30 min at 24 h before a 1-h oxygen-glucose deprivation (OGD) and a 24-h simulated reperfusion had a reduced lactate dehydrogenase release. Similarly, this OGD and simulated reperfusion-induced lactate dehydrogenase release was attenuated by exposing the neuronal cultures to 2% isoflurane for 1 h at various times after the onset of the simulated reperfusion (isoflurane postconditioning). The combination of isoflurane preconditioning and postconditioning induced a better neuroprotection than either alone. Inhibition of the calcium/calmodulin-dependent protein kinase II (CaMKII), inhibition of N-methyl D-aspartate (NMDA) receptors, or activation of adenosine A2A receptors resulted in reduction of the OGD and simulated reperfusion-induced cell injury. The combination of CaMKII inhibition and isoflurane preconditioning or postconditioning did not provide better protection than CaMKII inhibition, isoflurane preconditioning, or isoflurane postconditioning alone. The combination of NMDA receptor inhibition and isoflurane postconditioning was not better than NMDA receptor inhibition or isoflurane postconditioning alone for neuroprotection. However, the combination of adenosine A2A receptor activation with either isoflurane preconditioning or isoflurane postconditioning induced a better neuroprotective effect than adenosine A2A receptor activation, isoflurane preconditioning, or isoflurane postconditioning alone. The combination of NMDA receptor inhibition and isoflurane preconditioning caused a better neuroprotective effect than NMDA receptor inhibition or isoflurane preconditioning alone. These results suggest that isoflurane preconditioning- and postconditioning-induced neuroprotection can be additive. Isoflurane preconditioning and isoflurane postconditioning may involve CaMKII inhibition, but may not involve adenosine A2A receptor activation. Inhibition of NMDA receptors may mediate the effects of isoflurane postconditioning, but not isoflurane preconditioning.

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Section: Discussionmentioning

confidence: 99%

Isoflurane preconditioning and postconditioning in rat hippocampal neurons

McMurtrey

Zuo

2010

Brain Research

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“…Protection was still preserved when application of Postcon was delayed 5 min after reperfusion, but with no protection after 10 min. Also, they found that additive neuroprotective effects on the spinal cord when preconditioning and Postcon were combined [105]. Song et al found that attenuation in spinal cord injury during 48 h of reperfusion with three 30/30 s cycles of Postcon is associated with upregulation of endogenous antioxidant enzymes activities [106].…”

Section: Reduction Of Spinal Cord and Brain Injurymentioning

confidence: 99%