{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T20:34:21Z","timestamp":1771014861531,"version":"3.50.1"},"reference-count":57,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2020,5,5]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Hyperoxia during cardiopulmonary resuscitation (CPR) may lead to oxidative injury from mitochondrial\u2010derived reactive oxygen species, despite guidelines recommending 1.0 inspired oxygen during\n              <jats:styled-content style=\"fixed-case\">CPR<\/jats:styled-content>\n              . We hypothesized exposure to 1.0 inspired oxygen during\n              <jats:styled-content style=\"fixed-case\">CPR<\/jats:styled-content>\n              would result in cerebral hyperoxia, higher mitochondrial\u2010derived reactive oxygen species, increased oxidative injury, and similar survival compared with those exposed to 21% oxygen.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Four\u2010week\u2010old piglets (n=25) underwent asphyxial cardiac arrest followed by randomization and blinding to\n              <jats:styled-content style=\"fixed-case\">CPR<\/jats:styled-content>\n              with 0.21 (n=10) or 1.0 inspired oxygen (n=10) through 10\u00a0minutes post return of spontaneous circulation. Sham was n=5. Survivors received 4\u00a0hours of protocolized postarrest care, whereupon brain was obtained for mitochondrial analysis and neuropathology. Groups were compared using Kruskal\u2010Wallis test, Wilcoxon rank\u2010sum test, and generalized estimating equations regression models. Both 1.0 and 0.21 groups were similar in systemic hemodynamics and cerebral blood flow, as well as survival (8\/10). The 1.0 animals had relative cerebral hyperoxia during\n              <jats:styled-content style=\"fixed-case\">CPR<\/jats:styled-content>\n              and immediately following return of spontaneous circulation (brain tissue oxygen tension, 85% [interquartile range, 72%\u2013120%] baseline in 0.21 animals versus 697% [interquartile range, 515%\u2013721%] baseline in 1.0 animals;\n              <jats:italic>P<\/jats:italic>\n              =0.001 at 10\u00a0minutes postarrest). Cerebral mitochondrial reactive oxygen species production was higher in animals treated with 1.0 compared with 0.21 (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.03). Exposure to 1.0 oxygen led to increased cerebral oxidative injury to proteins and lipids, as evidenced by significantly higher protein carbonyls and 4\u2010hydroxynoneals compared with 0.21 (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05) and sham (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Exposure to 1.0 inspired oxygen during\n              <jats:styled-content style=\"fixed-case\">CPR<\/jats:styled-content>\n              caused cerebral hyperoxia during resuscitation, and resultant increased mitochondrial\u2010derived reactive oxygen species and oxidative injury following cardiac arrest.\n            <\/jats:p>\n          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