{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T03:21:08Z","timestamp":1773285668322,"version":"3.50.1"},"reference-count":24,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"21","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2018,11,6]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              After cardiopulmonary resuscitation, the protective effects of therapeutic hypothermia induced by conventional cooling are limited. Recently, esophageal cooling (\n              <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content>\n              ) has been shown to be an effective, easily performed approach to induce therapeutic hypothermia. In this study we investigated the efficacy of\n              <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content>\n              and its effects on early markers of postresuscitation cardiac and neurological injury in a porcine model of cardiac arrest.\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              Thirty\u2010two male domestic swine were randomized into 4 groups: sham control, normothermia, surface cooling, and\n              <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content>\n              . Sham animals underwent the surgical preparation only. Ventricular fibrillation was induced and untreated for 8\u00a0minutes while defibrillation was attempted after 5\u00a0minutes of cardiopulmonary resuscitation. At 5\u00a0minutes after resuscitation, therapeutic hypothermia was induced by either\n              <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content>\n              or surface cooling to reach a target temperature of 33\u00b0C until 24\u00a0hours postresuscitation, followed by a rewarming rate of 1\u00b0C\/h for 5\u00a0hours. The temperature was normally maintained in the control and normothermia groups. After resuscitation, a significantly faster decrease in blood temperature was observed in the\n              <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content>\n              group than in the surface cooling group (2.8\u00b10.7\u00b0C\/h versus 1.5\u00b10.4\u00b0C\/h;\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05). During the maintenance and rewarming phases the temperature was maintained at an even level between the 2 groups. Postresuscitation cardiac and neurological damage was significantly improved in the 2 hypothermic groups compared with the normothermia group; however, the protective effects were significantly greater in the\n              <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content>\n              group.\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              In a porcine model of cardiac arrest, faster hypothermia successfully induced by\n              <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content>\n              was significantly better than conventional cooling in improving early markers of postresuscitation cardiac and neurological injury.\n            <\/jats:p>\n          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