title: Combined exposure to hypercapnia and hypoxia provides its maximum neuroprotective effect during focal ischemic injury in the brain.
abstract: 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.
authors.affiliation: Department of Pathophysiology, Federal Agency for Health and Social Development, Altai State Medical University, Barnaul, Altai Region, Russia. Electronic address: pfiza_asmu@mail.ru.
authors.forename: Pavel
authors.initials: P
authors.lastname: Tregub
authors.affiliation: Department of Pathophysiology, Federal Agency for Health and Social Development, Altai State Medical University, Barnaul, Altai Region, Russia.
authors.forename: Vladimir
authors.initials: V
authors.lastname: Kulikov
authors.affiliation: Department of Histology, Federal Agency for Health and Social Development, Altai State Medical University, Barnaul, Altai Region, Russia.
authors.forename: Yuri
authors.initials: Y
authors.lastname: Motin
authors.affiliation: Department of Pathophysiology, Federal Agency for Health and Social Development, Altai State Medical University, Barnaul, Altai Region, Russia.
authors.forename: Andrey
authors.initials: A
authors.lastname: Bespalov
authors.affiliation: Department of Pathophysiology, Federal Agency for Health and Social Development, Altai State Medical University, Barnaul, Altai Region, Russia.
authors.forename: Ilya
authors.initials: I
authors.lastname: Osipov
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology*; D002545:Brain Ischemia / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D006935:Hypercapnia / Q000150:complications*; D002534:Hypoxia, Brain / Q000150:complications*; D008297:Male; D051381:Rats; D017208:Rats, Wistar
keywords: Focal stroke; hypercapnia; hypercapnic hypoxia; hypoxia; neuroprotection