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We studied the effects of hypoxic, hypercapnic, and hypercapnic-hypoxic exposures on brain tolerance to ischemia. All respiratory training modes had a neuroprotective effect, but the most pronounced effect was observed after exposure to hypercapnic hypoxia. Experimental stroke in rats preliminary exposed to hypercapnic hypoxia was associated with minimal neurological deficit and motor coordination disturbances in comparison with training modes.

We compared the intensity of apoptosis in the peri-infarction area of the brain after isolated and combined exposure to hypoxia and hypercapnia prior to focal ischemic stroke modeling. Hypoxia and hypercapnia reduced the number of TUNEL-positive cells in the peri-infarction area, and their combination was most effective in comparison with effects of isolated exposures. The maximum neuroprotective effect of combined exposure to hypoxia and hypercapnia in comparison with isolated exposures was determined by inhibition of apoptosis in the peri-infarction zone.

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We studied the expression of chaperone GRP-78 and transcription factor NF-kB during the development of ischemic tolerance of the brain after combined and isolated exposure to hypoxia and hypercapnia. Combined exposure to hypoxia and hypercapnia maximally increased the expression of chaperone GRP-78 and transcription factor NF-kB, while the formation of ischemia-induced tolerance under conditions of hypercapnic hypoxia can be associated with activation of adaptive stress mechanisms in the endoplasmic reticulum. Under these conditions, hypercapnia in combination with hypoxia is a priority factor for activation of GRP-78 and transcription factor NF-kB.