Ischemic tolerance in the rat neocortex following hypothermic preconditioning

Abstract

These findings indicate that hypothermic preconditioning induces a form of delayed tolerance to focal ischemic damage. The time course over which tolerance occurs and the ability of a protein synthesis inhibitor to block tolerance suggest that increased expression of one or more gene products is necessary to establish tissue tolerance following hypothermia. The attenuation of hypoxic injury in vitro following in vivo preconditioning indicates that tolerance is due, at least in part, to direct effects on the brain neuropil. Hypothermic preconditioning could provide a relatively low-risk approach for improving surgical outcome after invasive surgery, including high-risk neurological and cardiovascular procedures.

Deep Hypothermia Markedly Activates the Small Ubiquitin-Like Modifier Conjugation Pathway; Implications for the Fate of Cells Exposed to Transient Deep Hypothermic Cardiopulmonary Bypass

“…This would shorten the period of terminal depolarization and, thus, mitigate all pathologic processes triggered during the state of energy depletion and manifested after recovery from ischemia. However, transient hypothermia has been shown to induce rapid and delayed forms of tolerance to ischemic injury, suggesting that it can trigger an active process protecting cells from damage caused by ischemia (Nishio et al, 2000;Yunoki et al, 2002Yunoki et al, , 2003. The magnitude of tolerance induced by hypothermic preconditioning was found to be dependent on the depth of hypothermia with hypothermia set at 25.51C producing the most pronounced effects (Yunoki et al, 2002).…”

Arctic Ground Squirrel (Spermophilus Parryii) Hippocampal Neurons Tolerate Prolonged Oxygen—Glucose Deprivation and Maintain Baseline ERK1/2 and JNK Activation Despite Drastic ATP Loss

“…Regression analysis showed no correlation between the number of days spent in torpor immediately before euthanasia and sensitivity to 2 h OGD in hAGS (R 2 = 0.099, P = 0.13). The tolerance of ibeAGS to OGD may be because of the preconditioning effects of hypothermia experienced during previous hibernation bouts (Nishio et al, 2000). Hypothermic preconditioning has been reported to last less than 7 days in rats (Nishio et al, 2000); therefore, we tested hippocampal tissue collected from AGS during the summer months (July-August) that had not been torpid for at least 4 months and should no longer be affected by hypothermic preconditioning.…”

“…The tolerance of ibeAGS to OGD may be because of the preconditioning effects of hypothermia experienced during previous hibernation bouts (Nishio et al, 2000). Hypothermic preconditioning has been reported to last less than 7 days in rats (Nishio et al, 2000); therefore, we tested hippocampal tissue collected from AGS during the summer months (July-August) that had not been torpid for at least 4 months and should no longer be affected by hypothermic preconditioning. We found that baseline cell death increased to 50.9% ± 5.8% (P < 0.001 versus ibeAGS or hAGS), but similar to the winter animals, there was no increase in cell death in response to 30 mins OGD ( Figure 1C), suggesting that tolerance to OGD is not because of preconditioning effects of recent low body temperatures.…”

TNF-α and Microglial Hormetic Involvement in Neurological Health & Migraine

“…This suggests that EE, like other preconditioning stimuli (Barone et al 1998;Nishio et al 2000), requires new protein synthesis. The predominant effect of TNF-α is to alter gene expression (Abbas and Lichtman 2003).…”