Combined exposure to hypercapnia and hypoxia provides its maximum neuroprotective effect during focal ischemic injury in the brain.

BACKGROUND: In the present research, we compared the neuroprotective efficiency of combined and isolated exposure to hypoxia and hypercapnia preceding focal cerebral ischemic injury in rats. The study was conducted to verify the hypothesis of a possible increase in normobaric hypoxia (NbH; 90 mm Hg) efficiency when combined with permissive hypercapnia (PH; 50 mm Hg). METHODS: The rats from the test groups were subjected to a 15-fold exposure to NbH (90 mm Hg) and/or PH (50 mm Hg). After the 15th exposure, cerebral ischemic injury was induced by photochemical thrombosis. Seventy-two hours later, neurologic deficit was determined on the Neurological Severity Score scale and by the rotarod test, and the volume of cerebral infarction was measured after focal photochemical thrombosis. RESULTS: The neurologic deficit decreased most efficiently in rats that underwent PH and hypercapnic hypoxia (HH) exposure, whereas NbH had no impact on the neurologic status of the animals. On the contrary, motor coordination disturbances were minimal during exposure to hypoxia and HH. All respiratory interventions reduced the cerebral ischemic infarction volume in rats. The smallest infarction volumes were registered in the area of photochemical thrombosis in rats from the hypercapnic-hypoxic impact group, whereas exposure to NbH or PH did not show any cross difference. CONCLUSIONS: The impact of PH has greater neuroprotective potential compared with NbH. Thus, we can assume that hypercapnia is a predominant factor in providing neuroprotection in combination with hypoxia.

Tolerance to acute hypoxia maximally increases in case of joint effect of normobaric hypoxia and permissive hypercapnia in rats.

INTRODUCTION: We studied the comparative efficacy of independent and combined effects of normobaric hypoxia (90mmHg) and permissive hypercapnia (50mmHg) in increasing the tolerance of rats to acute hypobaric hypoxia. METHODS: We determined the time to loss of pose and life duration as a measure to assess the degree of tolerance of animals to hypobaric hypoxia by exposing them to an altitude of 11,500m (barometric=180mmHg). RESULTS: Exposure to hypercapnic hypoxia increased the tolerance to acute hypobaric hypoxia compared to exposure to normobaric hypoxia or permissive hypercapnia alone. DISCUSSION: The positive effects of hypercapnia and hypercapnic hypoxia occurred after one exposure, and increasing the number of exposures proportionally increased the tolerance to acute hypobaric hypoxia. The effect of permissive hypercapnia on increasing the tolerance to acute hypobaric hypoxia was found to be significantly greater than that of exposure to normobaric hypoxia. Therefore, we propose that hypercapnia is the dominant factor in increasing tolerance to acute hypobaric hypoxia. CONCLUSION: Tolerance to acute hypoxia maximally increases in case of joint effect of normobaric hypoxia and permissive hypercapnia.