Therapeutic Hypothermia Reduces Oxidative Damage and Alters Antioxidant Defenses after Cardiac Arrest
After cardiac arrest, organ damage consequent to ischemia-reperfusion has been attributed to oxidative stress. Mild therapeutic hypothermia has been applied to reduce this damage, and it may reduce oxidative damage as well. This study aimed to compare oxidative damage and antioxidant defenses in pat...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2017-01, Vol.2017 (2017), p.1-10 |
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| creator | Guerra, Maria Cristina Oliveira, Vanessa M. Riveiro, Diego F. M. Vieira, Silvia R. R. Benfato, Mara S. da Silva, Ana Carolina A. Verona, Cleber Mahl, Camila D. Putti, Jordana S. Behling, Camile S. Heemann, Fernanda M. Medeiros, Tássia M. Hackenhaar, Fernanda S. Gonçalves, Carlos Alberto |
| description | After cardiac arrest, organ damage consequent to ischemia-reperfusion has been attributed to oxidative stress. Mild therapeutic hypothermia has been applied to reduce this damage, and it may reduce oxidative damage as well. This study aimed to compare oxidative damage and antioxidant defenses in patients treated with controlled normothermia versus mild therapeutic hypothermia during postcardiac arrest syndrome. The sample consisted of 31 patients under controlled normothermia (36°C) and 11 patients treated with 24 h mild therapeutic hypothermia (33°C), victims of in- or out-of-hospital cardiac arrest. Parameters were assessed at 6, 12, 36, and 72 h after cardiac arrest in the central venous blood samples. Hypothermic and normothermic patients had similar S100B levels, a biomarker of brain injury. Xanthine oxidase activity is similar between hypothermic and normothermic patients; however, it decreases posthypothermia treatment. Xanthine oxidase activity is positively correlated with lactate and S100B and inversely correlated with pH, calcium, and sodium levels. Hypothermia reduces malondialdehyde and protein carbonyl levels, markers of oxidative damage. Concomitantly, hypothermia increases the activity of erythrocyte antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione S-transferase while decreasing the activity of serum paraoxonase-1. These findings suggest that mild therapeutic hypothermia reduces oxidative damage and alters antioxidant defenses in postcardiac arrest patients. |
| doi_str_mv | 10.1155/2017/8704352 |
| format | Article |
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M. ; Vieira, Silvia R. R. ; Benfato, Mara S. ; da Silva, Ana Carolina A. ; Verona, Cleber ; Mahl, Camila D. ; Putti, Jordana S. ; Behling, Camile S. ; Heemann, Fernanda M. ; Medeiros, Tássia M. ; Hackenhaar, Fernanda S. ; Gonçalves, Carlos Alberto</creator><contributor>Hrelia, Silvana</contributor><creatorcontrib>Guerra, Maria Cristina ; Oliveira, Vanessa M. ; Riveiro, Diego F. M. ; Vieira, Silvia R. R. ; Benfato, Mara S. ; da Silva, Ana Carolina A. ; Verona, Cleber ; Mahl, Camila D. ; Putti, Jordana S. ; Behling, Camile S. ; Heemann, Fernanda M. ; Medeiros, Tássia M. ; Hackenhaar, Fernanda S. ; Gonçalves, Carlos Alberto ; Hrelia, Silvana</creatorcontrib><description>After cardiac arrest, organ damage consequent to ischemia-reperfusion has been attributed to oxidative stress. Mild therapeutic hypothermia has been applied to reduce this damage, and it may reduce oxidative damage as well. This study aimed to compare oxidative damage and antioxidant defenses in patients treated with controlled normothermia versus mild therapeutic hypothermia during postcardiac arrest syndrome. The sample consisted of 31 patients under controlled normothermia (36°C) and 11 patients treated with 24 h mild therapeutic hypothermia (33°C), victims of in- or out-of-hospital cardiac arrest. Parameters were assessed at 6, 12, 36, and 72 h after cardiac arrest in the central venous blood samples. Hypothermic and normothermic patients had similar S100B levels, a biomarker of brain injury. Xanthine oxidase activity is similar between hypothermic and normothermic patients; however, it decreases posthypothermia treatment. Xanthine oxidase activity is positively correlated with lactate and S100B and inversely correlated with pH, calcium, and sodium levels. Hypothermia reduces malondialdehyde and protein carbonyl levels, markers of oxidative damage. Concomitantly, hypothermia increases the activity of erythrocyte antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione S-transferase while decreasing the activity of serum paraoxonase-1. These findings suggest that mild therapeutic hypothermia reduces oxidative damage and alters antioxidant defenses in postcardiac arrest patients.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2017/8704352</identifier><identifier>PMID: 28553435</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Antioxidants ; Antioxidants - metabolism ; Biomarkers - metabolism ; Body temperature ; Brain ; Brain - pathology ; Cardiac arrest ; Cardiopulmonary resuscitation ; Care and treatment ; Coma ; Cooling ; CPR ; Electrolytes ; Female ; Glutathione transferase ; Health aspects ; Heart Arrest - pathology ; Heart Arrest - therapy ; Heart rate ; Humans ; Hypothermia ; Hypothermia, Induced ; Hypoxia ; Injuries ; Intensive care ; Ischemia ; Laboratories ; Male ; Metabolism ; Middle Aged ; Out-of-Hospital Cardiac Arrest ; Oxidases ; Oxidative Stress ; Patients ; Proteins ; Rodents ; Superoxide ; Treatment Outcome ; Xanthine Oxidase - metabolism</subject><ispartof>Oxidative medicine and cellular longevity, 2017-01, Vol.2017 (2017), p.1-10</ispartof><rights>Copyright © 2017 Fernanda S. Hackenhaar et al.</rights><rights>COPYRIGHT 2017 John Wiley & Sons, Inc.</rights><rights>Copyright © 2017 Fernanda S. Hackenhaar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2017 Fernanda S. Hackenhaar et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-84ce5a8a31fa0fdda74c9f5eb8b319e7d4349c260c6dd999bc2a8edb57ed758c3</citedby><cites>FETCH-LOGICAL-c565t-84ce5a8a31fa0fdda74c9f5eb8b319e7d4349c260c6dd999bc2a8edb57ed758c3</cites><orcidid>0000-0001-5997-1926</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5434234/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5434234/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28553435$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Hrelia, Silvana</contributor><creatorcontrib>Guerra, Maria Cristina</creatorcontrib><creatorcontrib>Oliveira, Vanessa M.</creatorcontrib><creatorcontrib>Riveiro, Diego F. M.</creatorcontrib><creatorcontrib>Vieira, Silvia R. R.</creatorcontrib><creatorcontrib>Benfato, Mara S.</creatorcontrib><creatorcontrib>da Silva, Ana Carolina A.</creatorcontrib><creatorcontrib>Verona, Cleber</creatorcontrib><creatorcontrib>Mahl, Camila D.</creatorcontrib><creatorcontrib>Putti, Jordana S.</creatorcontrib><creatorcontrib>Behling, Camile S.</creatorcontrib><creatorcontrib>Heemann, Fernanda M.</creatorcontrib><creatorcontrib>Medeiros, Tássia M.</creatorcontrib><creatorcontrib>Hackenhaar, Fernanda S.</creatorcontrib><creatorcontrib>Gonçalves, Carlos Alberto</creatorcontrib><title>Therapeutic Hypothermia Reduces Oxidative Damage and Alters Antioxidant Defenses after Cardiac Arrest</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>After cardiac arrest, organ damage consequent to ischemia-reperfusion has been attributed to oxidative stress. Mild therapeutic hypothermia has been applied to reduce this damage, and it may reduce oxidative damage as well. This study aimed to compare oxidative damage and antioxidant defenses in patients treated with controlled normothermia versus mild therapeutic hypothermia during postcardiac arrest syndrome. The sample consisted of 31 patients under controlled normothermia (36°C) and 11 patients treated with 24 h mild therapeutic hypothermia (33°C), victims of in- or out-of-hospital cardiac arrest. Parameters were assessed at 6, 12, 36, and 72 h after cardiac arrest in the central venous blood samples. Hypothermic and normothermic patients had similar S100B levels, a biomarker of brain injury. Xanthine oxidase activity is similar between hypothermic and normothermic patients; however, it decreases posthypothermia treatment. Xanthine oxidase activity is positively correlated with lactate and S100B and inversely correlated with pH, calcium, and sodium levels. Hypothermia reduces malondialdehyde and protein carbonyl levels, markers of oxidative damage. Concomitantly, hypothermia increases the activity of erythrocyte antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione S-transferase while decreasing the activity of serum paraoxonase-1. These findings suggest that mild therapeutic hypothermia reduces oxidative damage and alters antioxidant defenses in postcardiac arrest patients.</description><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Biomarkers - metabolism</subject><subject>Body temperature</subject><subject>Brain</subject><subject>Brain - pathology</subject><subject>Cardiac arrest</subject><subject>Cardiopulmonary resuscitation</subject><subject>Care and treatment</subject><subject>Coma</subject><subject>Cooling</subject><subject>CPR</subject><subject>Electrolytes</subject><subject>Female</subject><subject>Glutathione transferase</subject><subject>Health aspects</subject><subject>Heart Arrest - pathology</subject><subject>Heart Arrest - therapy</subject><subject>Heart rate</subject><subject>Humans</subject><subject>Hypothermia</subject><subject>Hypothermia, Induced</subject><subject>Hypoxia</subject><subject>Injuries</subject><subject>Intensive care</subject><subject>Ischemia</subject><subject>Laboratories</subject><subject>Male</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Out-of-Hospital Cardiac Arrest</subject><subject>Oxidases</subject><subject>Oxidative Stress</subject><subject>Patients</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Superoxide</subject><subject>Treatment Outcome</subject><subject>Xanthine Oxidase - metabolism</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkUFv1DAQhS0Eou3CjTOyxAUJltpOnNgXpGhbKFKlSqicrYk92XWVOIudFPrv8WqXLXDiZFvvmzczfoS84uwD51KeC8brc1WzspDiCTnluhRLpnX59Hhn7IScpXTHWFWIkj8nJ0JJWeSCU4K3G4ywxXnyll49bMcpvwcP9Cu62WKiNz-9g8nfI72AAdZIITja9BPGRJsw-XGnh4leYIch5QLoskZXEJ0HS5sYMU0vyLMO-oQvD-eCfPt0ebu6Wl7ffP6yaq6XVlZyWqrSogQFBe-Adc5BXVrdSWxVW3CNtSuLUltRMVs5p7VurQCFrpU1uloqWyzIx73vdm4HdBbDFKE32-gHiA9mBG_-VoLfmPV4b2R2FvlHFuTtwSCO3-c8uRl8stj3EHCck-GaZUppUWX0zT_o3TjHkNczXGlV1UKw4pFaQ4_Gh27Mfe3O1DRSSiWZqlim3u8pG8eUInbHkTkzu5TNLmVzSDnjr_9c8wj_jjUD7_bAxgcHP_x_2mFmsINHmutKVLz4BRHeud4</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Guerra, Maria Cristina</creator><creator>Oliveira, Vanessa M.</creator><creator>Riveiro, Diego F. 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M.</au><au>Vieira, Silvia R. R.</au><au>Benfato, Mara S.</au><au>da Silva, Ana Carolina A.</au><au>Verona, Cleber</au><au>Mahl, Camila D.</au><au>Putti, Jordana S.</au><au>Behling, Camile S.</au><au>Heemann, Fernanda M.</au><au>Medeiros, Tássia M.</au><au>Hackenhaar, Fernanda S.</au><au>Gonçalves, Carlos Alberto</au><au>Hrelia, Silvana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Therapeutic Hypothermia Reduces Oxidative Damage and Alters Antioxidant Defenses after Cardiac Arrest</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>2017</volume><issue>2017</issue><spage>1</spage><epage>10</epage><pages>1-10</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>After cardiac arrest, organ damage consequent to ischemia-reperfusion has been attributed to oxidative stress. Mild therapeutic hypothermia has been applied to reduce this damage, and it may reduce oxidative damage as well. This study aimed to compare oxidative damage and antioxidant defenses in patients treated with controlled normothermia versus mild therapeutic hypothermia during postcardiac arrest syndrome. The sample consisted of 31 patients under controlled normothermia (36°C) and 11 patients treated with 24 h mild therapeutic hypothermia (33°C), victims of in- or out-of-hospital cardiac arrest. Parameters were assessed at 6, 12, 36, and 72 h after cardiac arrest in the central venous blood samples. Hypothermic and normothermic patients had similar S100B levels, a biomarker of brain injury. Xanthine oxidase activity is similar between hypothermic and normothermic patients; however, it decreases posthypothermia treatment. Xanthine oxidase activity is positively correlated with lactate and S100B and inversely correlated with pH, calcium, and sodium levels. Hypothermia reduces malondialdehyde and protein carbonyl levels, markers of oxidative damage. Concomitantly, hypothermia increases the activity of erythrocyte antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione S-transferase while decreasing the activity of serum paraoxonase-1. These findings suggest that mild therapeutic hypothermia reduces oxidative damage and alters antioxidant defenses in postcardiac arrest patients.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>28553435</pmid><doi>10.1155/2017/8704352</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-5997-1926</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Oxidative medicine and cellular longevity, 2017-01, Vol.2017 (2017), p.1-10 |
| issn | 1942-0900 1942-0994 |
| language | eng |
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| source | MEDLINE; PubMed Central Open Access; Wiley Online Library Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Antioxidants Antioxidants - metabolism Biomarkers - metabolism Body temperature Brain Brain - pathology Cardiac arrest Cardiopulmonary resuscitation Care and treatment Coma Cooling CPR Electrolytes Female Glutathione transferase Health aspects Heart Arrest - pathology Heart Arrest - therapy Heart rate Humans Hypothermia Hypothermia, Induced Hypoxia Injuries Intensive care Ischemia Laboratories Male Metabolism Middle Aged Out-of-Hospital Cardiac Arrest Oxidases Oxidative Stress Patients Proteins Rodents Superoxide Treatment Outcome Xanthine Oxidase - metabolism |
| title | Therapeutic Hypothermia Reduces Oxidative Damage and Alters Antioxidant Defenses after Cardiac Arrest |
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