{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T06:29:57Z","timestamp":1780381797278,"version":"3.54.1"},"reference-count":53,"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":[[2015,9,16]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Although advances in cardiopulmonary resuscitation have improved survival from cardiac arrest (\n              <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>\n              ), neurologic injury persists and impaired mitochondrial bioenergetics may be critical for targeted neuroresuscitation. The authors sought to determine if excellent cardiopulmonary resuscitation and postresuscitation care and good traditional survival rates result in persistently disordered cerebral mitochondrial bioenergetics in a porcine pediatric model of asphyxia\u2010associated ventricular fibrillation\n              <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>\n              .\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              After 7\u00a0minutes of asphyxia, followed by ventricular fibrillation, 5 female 1\u2010month\u2010old swine (4 sham) received blood pressure\u2013targeted care: titration of compression depth to systolic blood pressure of 90\u00a0mm\u00a0Hg and vasopressor administration to a coronary perfusion pressure &gt;20\u00a0mm\u00a0Hg. All animals received protocol\u2010based vasopressor support after return of spontaneous circulation for 4\u00a0hours before they were killed. The primary outcome was integrated mitochondrial electron transport system (\n              <jats:styled-content style=\"fixed-case\">ETS<\/jats:styled-content>\n              ) function.\n              <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>\n              animals displayed significantly decreased maximal, coupled oxidative phosphorylating respiration (\n              <jats:styled-content style=\"fixed-case\">\n                OXPHOS\n                <jats:sub>CI<\/jats:sub>\n              <\/jats:styled-content>\n              <jats:sub>+<\/jats:sub>\n              <jats:styled-content style=\"fixed-case\">\n                <jats:sub>CII<\/jats:sub>\n              <\/jats:styled-content>\n              ) in cortex (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.02) and hippocampus (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.02), as well as decreased phosphorylation and coupling efficiency (cortex,\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05; hippocampus,\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05). Complex I\u2013 and complex\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              \u2013driven respiration were both significantly decreased after\n              <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>\n              (cortex:\n              <jats:styled-content style=\"fixed-case\">\n                OXPHOS\n                <jats:sub>CI<\/jats:sub>\n              <\/jats:styled-content>\n              <jats:italic>P<\/jats:italic>\n              &lt;0.01,\n              <jats:styled-content style=\"fixed-case\">\n                ETS\n                <jats:sub>CII<\/jats:sub>\n              <\/jats:styled-content>\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05; hippocampus:\n              <jats:styled-content style=\"fixed-case\">\n                OXPHOS\n                <jats:sub>CI<\/jats:sub>\n              <\/jats:styled-content>\n              <jats:italic>P<\/jats:italic>\n              &lt;0.03,\n              <jats:styled-content style=\"fixed-case\">\n                ETS\n                <jats:sub>CII<\/jats:sub>\n              <\/jats:styled-content>\n              <jats:italic>P<\/jats:italic>\n              &lt;0.01). In the hippocampus, there was a significant decrease in maximal uncoupled, nonphosphorylating respiration (\n              <jats:styled-content style=\"fixed-case\">\n                ETS\n                <jats:sub>CI<\/jats:sub>\n              <\/jats:styled-content>\n              <jats:sub>+<\/jats:sub>\n              <jats:styled-content style=\"fixed-case\">\n                <jats:sub>CII<\/jats:sub>\n              <\/jats:styled-content>\n              ), as well as a 30% reduction in citrate synthase activity (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.04).\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              Mitochondria in both the cortex and hippocampus displayed significant alterations in respiratory function after\n              <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>\n              despite excellent cardiopulmonary resuscitation and postresuscitation care in asphyxia\u2010associated ventricular fibrillation\n              <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>\n              . Analysis of integrated\n              <jats:styled-content style=\"fixed-case\">ETS<\/jats:styled-content>\n              function identifies mitochondrial bioenergetic failure as a target for goal\u2010directed neuroresuscitation after\n              <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>\n              .\n              <jats:styled-content style=\"fixed-case\">IACUC<\/jats:styled-content>\n              Protocol:\n              <jats:styled-content style=\"fixed-case\">IAC<\/jats:styled-content>\n              13\u2010001023.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.115.002232","type":"journal-article","created":{"date-parts":[[2015,9,15]],"date-time":"2015-09-15T01:40:37Z","timestamp":1442281237000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":40,"title":["Persistently Altered Brain Mitochondrial Bioenergetics After Apparently Successful Resuscitation From Cardiac Arrest"],"prefix":"10.1161","volume":"4","author":[{"given":"Todd J.","family":"Kilbaugh","sequence":"first","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, The Children's Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert M.","family":"Sutton","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, The Children's Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Karlsson","sequence":"additional","affiliation":[{"name":"Mitochondrial Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magnus J.","family":"Hansson","sequence":"additional","affiliation":[{"name":"Mitochondrial Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maryam Y.","family":"Naim","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, The Children's Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan W.","family":"Morgan","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, The Children's Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George","family":"Bratinov","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, The Children's Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua W.","family":"Lampe","sequence":"additional","affiliation":[{"name":"Department of Emergency Medicine, The Hospital of the University of Pennsylvania, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vinay M.","family":"Nadkarni","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, The Children's Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lance B.","family":"Becker","sequence":"additional","affiliation":[{"name":"Department of Emergency Medicine, The Hospital of the University of Pennsylvania, University of Pennsylvania Perelman School of Medicine, 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