Neither Xenon nor Fentanyl Induces Neuroapoptosis in the Newborn Pig Brain
BACKGROUND:Some inhalation anesthetics increase apoptotic cell death in the developing brain. Xenon, an inhalation anesthetic, increases neuroprotection when combined with therapeutic hypothermia after hypoxic-ischemic brain injury in newborn animals. The authors, therefore, examined whether there w...
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| Veröffentlicht in: | Anesthesiology (Philadelphia) 2013-08, Vol.119 (2), p.345-357 |
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| creator | Sabir, Hemmen Bishop, Sarah Cohen, Nicki Maes, Elke Liu, Xun Dingley, John Thoresen, Marianne |
| description | BACKGROUND:Some inhalation anesthetics increase apoptotic cell death in the developing brain. Xenon, an inhalation anesthetic, increases neuroprotection when combined with therapeutic hypothermia after hypoxic-ischemic brain injury in newborn animals. The authors, therefore, examined whether there was any neuroapoptotic effect of breathing 50% xenon with continuous fentanyl sedation for 24 h at normothermia or hypothermia on newborn pigs.
METHODS:Twenty-six healthy pigs ( |
| doi_str_mv | 10.1097/ALN.0b013e318294934d |
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METHODS:Twenty-six healthy pigs (<24-h old) were randomized into four groups(1) 24 h of 50% inhaled xenon with fentanyl at hypothermia (Trec = 33.5°C), (2) 24 h of 50% inhaled xenon with fentanyl at normothermia (Trec = 38.5°C), (3) 24 h of fentanyl at normothermia, or (4) nonventilated juvenile controls at normothermia. Five additional nonrandomized pigs inhaled 2% isoflurane at normothermia for 24 h to verify any proapoptotic effect of inhalation anesthetics in our model. Pathological cells were morphologically assessed in cortex, putamen, hippocampus, thalamus, and white matter. To quantify the findings, immunostained cells (caspase-3 and terminal deoxynucleotidyl transferase–mediated deoxyuridine-triphosphate nick-end labeling) were counted in the same brain regions.
RESULTS:For groups (1) to (4), the total number of apoptotic cells was less than 5 per brain region, representing normal developmental neuroapoptosis. After immunostaining and cell counting, regression analysis showed that neither 50% xenon with fentanyl nor fentanyl alone increased neuroapoptosis. Isoflurane caused on average a 5- to 10-fold increase of immunostained cells.
CONCLUSION:At normothermia or hypothermia, neither 24 h of inhaled 50% xenon with fentanyl sedation nor fentanyl alone induces neuroapoptosis in the neonatal pig brain. Breathing 2% isoflurane increases neuroapoptosis in neonatal pigs.</description><identifier>ISSN: 0003-3022</identifier><identifier>EISSN: 1528-1175</identifier><identifier>DOI: 10.1097/ALN.0b013e318294934d</identifier><identifier>PMID: 23591070</identifier><identifier>CODEN: ANESAV</identifier><language>eng</language><publisher>Hagerstown, MD: American Society of Anesthesiologists, Inc</publisher><subject>Anesthesia ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Anesthetics, Inhalation - pharmacology ; Anesthetics, Intravenous - pharmacology ; Animals ; Animals, Newborn ; Apoptosis - drug effects ; Biological and medical sciences ; Body Temperature ; Brain - drug effects ; Disease Models, Animal ; Fentanyl - pharmacology ; Hypothermia, Induced ; Medical sciences ; Neuroprotective Agents - pharmacology ; Swine ; Xenon - pharmacology</subject><ispartof>Anesthesiology (Philadelphia), 2013-08, Vol.119 (2), p.345-357</ispartof><rights>2013 American Society of Anesthesiologists, Inc.</rights><rights>2014 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c432d-f074d9b5a756b86df6a8d8d3d87e4fdda410389e8a496ac1924ac12f7e1be3873</citedby><cites>FETCH-LOGICAL-c432d-f074d9b5a756b86df6a8d8d3d87e4fdda410389e8a496ac1924ac12f7e1be3873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27618698$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23591070$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sabir, Hemmen</creatorcontrib><creatorcontrib>Bishop, Sarah</creatorcontrib><creatorcontrib>Cohen, Nicki</creatorcontrib><creatorcontrib>Maes, Elke</creatorcontrib><creatorcontrib>Liu, Xun</creatorcontrib><creatorcontrib>Dingley, John</creatorcontrib><creatorcontrib>Thoresen, Marianne</creatorcontrib><title>Neither Xenon nor Fentanyl Induces Neuroapoptosis in the Newborn Pig Brain</title><title>Anesthesiology (Philadelphia)</title><addtitle>Anesthesiology</addtitle><description>BACKGROUND:Some inhalation anesthetics increase apoptotic cell death in the developing brain. Xenon, an inhalation anesthetic, increases neuroprotection when combined with therapeutic hypothermia after hypoxic-ischemic brain injury in newborn animals. The authors, therefore, examined whether there was any neuroapoptotic effect of breathing 50% xenon with continuous fentanyl sedation for 24 h at normothermia or hypothermia on newborn pigs.
METHODS:Twenty-six healthy pigs (<24-h old) were randomized into four groups(1) 24 h of 50% inhaled xenon with fentanyl at hypothermia (Trec = 33.5°C), (2) 24 h of 50% inhaled xenon with fentanyl at normothermia (Trec = 38.5°C), (3) 24 h of fentanyl at normothermia, or (4) nonventilated juvenile controls at normothermia. Five additional nonrandomized pigs inhaled 2% isoflurane at normothermia for 24 h to verify any proapoptotic effect of inhalation anesthetics in our model. Pathological cells were morphologically assessed in cortex, putamen, hippocampus, thalamus, and white matter. To quantify the findings, immunostained cells (caspase-3 and terminal deoxynucleotidyl transferase–mediated deoxyuridine-triphosphate nick-end labeling) were counted in the same brain regions.
RESULTS:For groups (1) to (4), the total number of apoptotic cells was less than 5 per brain region, representing normal developmental neuroapoptosis. After immunostaining and cell counting, regression analysis showed that neither 50% xenon with fentanyl nor fentanyl alone increased neuroapoptosis. Isoflurane caused on average a 5- to 10-fold increase of immunostained cells.
CONCLUSION:At normothermia or hypothermia, neither 24 h of inhaled 50% xenon with fentanyl sedation nor fentanyl alone induces neuroapoptosis in the neonatal pig brain. Breathing 2% isoflurane increases neuroapoptosis in neonatal pigs.</description><subject>Anesthesia</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Anesthetics, Inhalation - pharmacology</subject><subject>Anesthetics, Intravenous - pharmacology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Body Temperature</subject><subject>Brain - drug effects</subject><subject>Disease Models, Animal</subject><subject>Fentanyl - pharmacology</subject><subject>Hypothermia, Induced</subject><subject>Medical sciences</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Swine</subject><subject>Xenon - pharmacology</subject><issn>0003-3022</issn><issn>1528-1175</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LxDAQhoMoun78A5FcBC_VfLVJjrr4ybJ6UPBW0mbqVrvJmrQs_nsjuyp48JIhw_PODA9Ch5ScUqLl2flkekoqQjlwqpgWmgu7gUY0ZyqjVOabaEQI4RknjO2g3Rhf01fmXG2jHcZzTYkkI3Q3hbafQcDP4LzDzgd8Ba437qPDt84ONUQ8hSF4s_CL3sc24tbhlEjdZeWDww_tC74IpnX7aKsxXYSDdd1DT1eXj-ObbHJ_fTs-n2S14MxmDZHC6io3Mi8qVdimMMoqy62SIBprjaCEKw3KCF2Ymmom0ssaCbQCriTfQyeruYvg3weIfTlvYw1dZxz4IZZUcM6kyJVIqFihdfAxBmjKRWjnJnyUlJRfFstksfxrMcWO1huGag72J_StLQHHa8DE2nRNMK5u4y8nC6oKrRKnVtzSdz2E-NYNSwjlDEzXz_6_4RPMWoyl</recordid><startdate>201308</startdate><enddate>201308</enddate><creator>Sabir, Hemmen</creator><creator>Bishop, Sarah</creator><creator>Cohen, Nicki</creator><creator>Maes, Elke</creator><creator>Liu, Xun</creator><creator>Dingley, John</creator><creator>Thoresen, Marianne</creator><general>American Society of Anesthesiologists, Inc</general><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201308</creationdate><title>Neither Xenon nor Fentanyl Induces Neuroapoptosis in the Newborn Pig Brain</title><author>Sabir, Hemmen ; Bishop, Sarah ; Cohen, Nicki ; Maes, Elke ; Liu, Xun ; Dingley, John ; Thoresen, Marianne</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c432d-f074d9b5a756b86df6a8d8d3d87e4fdda410389e8a496ac1924ac12f7e1be3873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Anesthesia</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Anesthetics, Inhalation - pharmacology</topic><topic>Anesthetics, Intravenous - pharmacology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Body Temperature</topic><topic>Brain - drug effects</topic><topic>Disease Models, Animal</topic><topic>Fentanyl - pharmacology</topic><topic>Hypothermia, Induced</topic><topic>Medical sciences</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Swine</topic><topic>Xenon - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sabir, Hemmen</creatorcontrib><creatorcontrib>Bishop, Sarah</creatorcontrib><creatorcontrib>Cohen, Nicki</creatorcontrib><creatorcontrib>Maes, Elke</creatorcontrib><creatorcontrib>Liu, Xun</creatorcontrib><creatorcontrib>Dingley, John</creatorcontrib><creatorcontrib>Thoresen, Marianne</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Anesthesiology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sabir, Hemmen</au><au>Bishop, Sarah</au><au>Cohen, Nicki</au><au>Maes, Elke</au><au>Liu, Xun</au><au>Dingley, John</au><au>Thoresen, Marianne</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neither Xenon nor Fentanyl Induces Neuroapoptosis in the Newborn Pig Brain</atitle><jtitle>Anesthesiology (Philadelphia)</jtitle><addtitle>Anesthesiology</addtitle><date>2013-08</date><risdate>2013</risdate><volume>119</volume><issue>2</issue><spage>345</spage><epage>357</epage><pages>345-357</pages><issn>0003-3022</issn><eissn>1528-1175</eissn><coden>ANESAV</coden><abstract>BACKGROUND:Some inhalation anesthetics increase apoptotic cell death in the developing brain. Xenon, an inhalation anesthetic, increases neuroprotection when combined with therapeutic hypothermia after hypoxic-ischemic brain injury in newborn animals. The authors, therefore, examined whether there was any neuroapoptotic effect of breathing 50% xenon with continuous fentanyl sedation for 24 h at normothermia or hypothermia on newborn pigs.
METHODS:Twenty-six healthy pigs (<24-h old) were randomized into four groups(1) 24 h of 50% inhaled xenon with fentanyl at hypothermia (Trec = 33.5°C), (2) 24 h of 50% inhaled xenon with fentanyl at normothermia (Trec = 38.5°C), (3) 24 h of fentanyl at normothermia, or (4) nonventilated juvenile controls at normothermia. Five additional nonrandomized pigs inhaled 2% isoflurane at normothermia for 24 h to verify any proapoptotic effect of inhalation anesthetics in our model. Pathological cells were morphologically assessed in cortex, putamen, hippocampus, thalamus, and white matter. To quantify the findings, immunostained cells (caspase-3 and terminal deoxynucleotidyl transferase–mediated deoxyuridine-triphosphate nick-end labeling) were counted in the same brain regions.
RESULTS:For groups (1) to (4), the total number of apoptotic cells was less than 5 per brain region, representing normal developmental neuroapoptosis. After immunostaining and cell counting, regression analysis showed that neither 50% xenon with fentanyl nor fentanyl alone increased neuroapoptosis. Isoflurane caused on average a 5- to 10-fold increase of immunostained cells.
CONCLUSION:At normothermia or hypothermia, neither 24 h of inhaled 50% xenon with fentanyl sedation nor fentanyl alone induces neuroapoptosis in the neonatal pig brain. Breathing 2% isoflurane increases neuroapoptosis in neonatal pigs.</abstract><cop>Hagerstown, MD</cop><pub>American Society of Anesthesiologists, Inc</pub><pmid>23591070</pmid><doi>10.1097/ALN.0b013e318294934d</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anesthesia Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Anesthetics, Inhalation - pharmacology Anesthetics, Intravenous - pharmacology Animals Animals, Newborn Apoptosis - drug effects Biological and medical sciences Body Temperature Brain - drug effects Disease Models, Animal Fentanyl - pharmacology Hypothermia, Induced Medical sciences Neuroprotective Agents - pharmacology Swine Xenon - pharmacology |
| title | Neither Xenon nor Fentanyl Induces Neuroapoptosis in the Newborn Pig Brain |
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