Effect of profound hypothermia during circulatory arrest on neurologic injury and apoptotic repressor protein Bcl-2 expression in an acute porcine model

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dc.contributor.authorAnaniadou, O. G.en
dc.contributor.authorBibou, K.en
dc.contributor.authorDrossos, G. E.en
dc.contributor.authorCharchanti, A.en
dc.contributor.authorBai, M.en
dc.contributor.authorHaj-Yahia, S.en
dc.contributor.authorAnagnostopoulos, C. E.en
dc.contributor.authorJohnson, E. O.en
dc.date.accessioned2015-11-24T19:22:35Z
dc.date.available2015-11-24T19:22:35Z
dc.identifier.issn1097-685X-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22175
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectApoptosis/physiologyen
dc.subjectBrain Diseases/etiology/*metabolismen
dc.subjectCardiopulmonary Bypass/adverse effectsen
dc.subjectCirculatory Arrest, Deep Hypothermia Induced/*adverse effectsen
dc.subjectDisease Models, Animalen
dc.subjectHippocampus/physiopathologyen
dc.subjectHypothermia, Induced/adverse effectsen
dc.subjectIn Situ Nick-End Labelingen
dc.subjectMaleen
dc.subjectNeocortex/physiopathologyen
dc.subjectProto-Oncogene Proteins c-bcl-2/*biosynthesisen
dc.subjectSwineen
dc.titleEffect of profound hypothermia during circulatory arrest on neurologic injury and apoptotic repressor protein Bcl-2 expression in an acute porcine modelen
heal.abstractOBJECTIVES: We reported that the neocortex and hippocampus are selectively vulnerable to injury in an acute porcine model of hypothermic circulatory arrest at 18 degrees C. We hypothesize that further cooling to 10 degrees C could reduce neurologic injury in these regions. To further elucidate the mechanisms of neurologic injury and protection, we assessed the expression of the anti-apoptotic protein Bcl-2. METHODS: Twelve piglets underwent 75 minutes of hypothermic circulatory arrest at 18 degrees C (n = 6) and 10 degrees C (n = 6). After gradual rewarming and reperfusion, animals were put to death and brains were perfusion-fixed and cryopreserved. Regional patterns of neuronal apoptosis after hypothermic circulatory arrest were characterized by in situ DNA fragmentation with terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) histochemistry. Bcl-2 protein expression was characterized with immunohistochemistry. Statistical comparisons were made by t test, analysis of variance, and Mann-Whitney U test, as appropriate. RESULTS: Concentrations of TUNEL(+) cells were significantly lower after profound hypothermia at 10 degrees C compared with 18 degrees C hypothermia in the sensory and motor neocortex and hippocampus (t test, P < .0001; P < .006; P < .006, respectively). Positive Bcl-2 immunostaining was observed only in the motor and sensory neocortex and hippocampus after 18 degrees C hypothermic circulatory arrest. Profound cooling to 10 degrees C resulted in a significant increase in Bcl-2 immunostaining in the motor and sensory cortex as compared with 18 degrees C (Mann-Whitney U test, P < .05). CONCLUSIONS: Deep hypothermia at 10 degrees C protects the neocortex and hippocampus from insult during hypothermic circulatory arrest as suggested by significantly reduced TUNEL(+) staining in these areas. Although a concomitant increase in Bcl-2 expression was observed in the neocortex at 10 degrees C, it remains unclear whether profound hypothermia deters from neuronal injury by activation of the anti-apoptotic protein Bcl-2.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primary10.1016/j.jtcvs.2006.10.045-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/17382626-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0022522306020861/1-s2.0-S0022522306020861-main.pdf?_tid=ed4d9b92bfe65461b59105b959c4426a&acdnat=1334046134_2c406b7ad2bfa969ec116fe5a5193ecc-
heal.journalNameJ Thorac Cardiovasc Surgen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2007-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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