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Hypoxia and hypercapnia were induced with low O\n                      <jats:sub>2<\/jats:sub>\n                      and high CO\n                      <jats:sub>2<\/jats:sub>\n                      respectively. Oxygen partial pressure (PO\n                      <jats:sub>2<\/jats:sub>\n                      ) and pH were measured with microsensors within the brain and subcutaneous (\u201cbody\u201d) tissue. Blood lactate was measured after asphyxia.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Brain and body PO\n                      <jats:sub>2<\/jats:sub>\n                      fell to apparent zero with little recovery during 5% O\n                      <jats:sub>2<\/jats:sub>\n                      asphyxia and 5% or 9% O\n                      <jats:sub>2<\/jats:sub>\n                      hypoxia, and increased more than twofold during 20% CO\n                      <jats:sub>2<\/jats:sub>\n                      hypercapnia. Unlike body PO\n                      <jats:sub>2<\/jats:sub>\n                      , brain PO\n                      <jats:sub>2<\/jats:sub>\n                      recovered rapidly to control after a transient fall (rat), or was slightly higher than control (guinea pig) during 9% O\n                      <jats:sub>2<\/jats:sub>\n                      asphyxia. Asphyxia (5% O\n                      <jats:sub>2<\/jats:sub>\n                      ) induced a respiratory acidosis paralleled by a progressive metabolic (lact)acidosis that was much smaller within than outside the brain. Hypoxia (5% O\n                      <jats:sub>2<\/jats:sub>\n                      ) produced a brain\u2010confined alkalosis. Hypercapnia outlasting asphyxia suppressed pH recovery and prolonged the post\u2010asphyxia PO\n                      <jats:sub>2<\/jats:sub>\n                      overshoot. All pH changes were accompanied by consistent shifts in the blood\u2010brain barrier potential.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Regardless of brain maturation stage, hypercapnia can restore brain PO\n                      <jats:sub>2<\/jats:sub>\n                      and protect the brain against metabolic acidosis despite compromised oxygen availability during asphyxia. This effect extends to the recovery phase if normocapnia is restored slowly, and it is absent during hypoxia, demonstrating that exposure to hypoxia does not mimic asphyxia.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apha.13467","type":"journal-article","created":{"date-parts":[[2020,3,16]],"date-time":"2020-03-16T04:16:37Z","timestamp":1584332197000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":41,"title":["Endogenous brain\u2010sparing responses in brain pH and PO\n                    <sub>2<\/sub>\n                    in a rodent model of birth asphyxia"],"prefix":"10.1111","volume":"229","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0793-2639","authenticated-orcid":false,"given":"Alexey S.","family":"Pospelov","sequence":"first","affiliation":[{"name":"Faculty of Biological and Environmental Sciences, Molecular and Integrative Biosciences University of Helsinki Helsinki 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