Hyperbaric oxygen therapy protects the liver from apoptosis caused by ischemia-reperfusion injury in rats
Purpose: The present paper aimed to investigate the role of hyperbaric oxygen treatment (HBO) and the apoptosis in rat liver ischemia‐reperfusion injury (IRI). Methods: Thirty‐seven male Wistar rats were subjected to 30 minutes of hepatic ischemia and 30 minutes of reperfusion and randomly distribut...
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Veröffentlicht in: | Microsurgery 2009-01, Vol.29 (7), p.578-583 |
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creator | Chaves, José C. Fagundes, Djalma J. Simões, Manuel De J. Bertoletto, Paulo R. Oshima, Celina T. F. Taha, Murched O. Simões, Ricardo S. Fagundes, Anna L. N. |
description | Purpose:
The present paper aimed to investigate the role of hyperbaric oxygen treatment (HBO) and the apoptosis in rat liver ischemia‐reperfusion injury (IRI).
Methods:
Thirty‐seven male Wistar rats were subjected to 30 minutes of hepatic ischemia and 30 minutes of reperfusion and randomly distributed into six groups: G‐I/R (n = 8), control without HBO; G‐HBO/I (n = 8), HBO only during the ischemia period; G‐HBO/R (n = 8), HBO only during the reperfusion period; G‐HBO‐I/R (n = 8), HBO during both the ischemia and reperfusion periods; G‐Sh (n = 3), HBO without ischemia or reperfusion as sham group; G‐C (n = 2) for control of current apoptosis expression on the normal liver tissue. HBO was carried out using a transparent, cylindrical acrylic chamber with a pressure of 2.0 ATA. Hepatic samples were stained for caspase‐3 cleavage.
Results:
Apoptotic cells were identified in all groups. In the hepatic specimens of animals HBO‐treated during ischemia (GHBO‐I), there was a significant decrease (P < 0.001) in the number of cells undergoing apoptosis (1.62 ± 0.91). The apoptotic index showed no significant difference in the animals HBO‐treated during ischemia/reperfusion (5.75 ± 1.28) compared with the G‐I/R (3.5 ± 0.75), which had no HBO treatment. The apoptosis index (11.25 ± 1.90) was significantly higher (P < 0.01) in HBO‐treated animals during the reperfusion period when compared with any of the other groups.
Conclusion:
A favorable effect was obtained when hyperbaric oxygen was administered early during ischemia. The hyperbaric oxygen in later periods of reperfusion was associated with a more severe apoptosis index. © 2009 Wiley‐Liss, Inc. Microsurgery 2009. |
doi_str_mv | 10.1002/micr.20664 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_734081955</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>734081955</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3664-6d539f3da34751979137d5345caf63c212ca0c5d2df115666e6942e94579b273</originalsourceid><addsrcrecordid>eNp9kM1O3DAUhS3UCgbohgdA3lWqFOqf2I6XdFQGBAWJjsTS8jg3YMhf7aSQt8fDDHTXlaXr73469yB0RMkJJYR9b7wLJ4xIme-gGSW6yJgS7BOaEcWLjJJC7KH9GB8JIVorvYv2qOZaF6qYIX8-9RBWNniHu5fpHlo8PECw_YT70A3ghrge4Nr_hYCr0DXY9l0_dNFH7OwYocSrCfvoHqDxNguQdNUYfddi3z6OIf21ONghHqLPla0jfNm-B2h59nM5P8-ubhYX89OrzPF0QSZLwXXFS8tzJWiKS7lKo1w4W0nuGGXOEidKVlaUCiklSJ0z0LlQesUUP0BfN9oU_88IcTBNCgd1bVvoxmgUz0lBtRCJ_LYhXehiDFCZPvjGhslQYtbFmnWx5q3YBB9vteOqgfIfum0yAXQDPPsapv-ozK-L-e27NNvs-DjAy8eODU9GKq6EubtemAVd_r7ML3-YO_4KmxaTyA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>734081955</pqid></control><display><type>article</type><title>Hyperbaric oxygen therapy protects the liver from apoptosis caused by ischemia-reperfusion injury in rats</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Chaves, José C. ; Fagundes, Djalma J. ; Simões, Manuel De J. ; Bertoletto, Paulo R. ; Oshima, Celina T. F. ; Taha, Murched O. ; Simões, Ricardo S. ; Fagundes, Anna L. N.</creator><creatorcontrib>Chaves, José C. ; Fagundes, Djalma J. ; Simões, Manuel De J. ; Bertoletto, Paulo R. ; Oshima, Celina T. F. ; Taha, Murched O. ; Simões, Ricardo S. ; Fagundes, Anna L. N.</creatorcontrib><description>Purpose:
The present paper aimed to investigate the role of hyperbaric oxygen treatment (HBO) and the apoptosis in rat liver ischemia‐reperfusion injury (IRI).
Methods:
Thirty‐seven male Wistar rats were subjected to 30 minutes of hepatic ischemia and 30 minutes of reperfusion and randomly distributed into six groups: G‐I/R (n = 8), control without HBO; G‐HBO/I (n = 8), HBO only during the ischemia period; G‐HBO/R (n = 8), HBO only during the reperfusion period; G‐HBO‐I/R (n = 8), HBO during both the ischemia and reperfusion periods; G‐Sh (n = 3), HBO without ischemia or reperfusion as sham group; G‐C (n = 2) for control of current apoptosis expression on the normal liver tissue. HBO was carried out using a transparent, cylindrical acrylic chamber with a pressure of 2.0 ATA. Hepatic samples were stained for caspase‐3 cleavage.
Results:
Apoptotic cells were identified in all groups. In the hepatic specimens of animals HBO‐treated during ischemia (GHBO‐I), there was a significant decrease (P < 0.001) in the number of cells undergoing apoptosis (1.62 ± 0.91). The apoptotic index showed no significant difference in the animals HBO‐treated during ischemia/reperfusion (5.75 ± 1.28) compared with the G‐I/R (3.5 ± 0.75), which had no HBO treatment. The apoptosis index (11.25 ± 1.90) was significantly higher (P < 0.01) in HBO‐treated animals during the reperfusion period when compared with any of the other groups.
Conclusion:
A favorable effect was obtained when hyperbaric oxygen was administered early during ischemia. The hyperbaric oxygen in later periods of reperfusion was associated with a more severe apoptosis index. © 2009 Wiley‐Liss, Inc. Microsurgery 2009.</description><identifier>ISSN: 0738-1085</identifier><identifier>EISSN: 1098-2752</identifier><identifier>DOI: 10.1002/micr.20664</identifier><identifier>PMID: 19399878</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Apoptosis - physiology ; Caspase 3 - metabolism ; Disease Models, Animal ; Hyperbaric Oxygenation - methods ; Immunohistochemistry ; Liver - enzymology ; Liver - physiopathology ; Male ; Rats ; Rats, Wistar ; Reperfusion Injury - physiopathology ; Reperfusion Injury - prevention & control ; Time Factors</subject><ispartof>Microsurgery, 2009-01, Vol.29 (7), p.578-583</ispartof><rights>Copyright © 2009 Wiley‐Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3664-6d539f3da34751979137d5345caf63c212ca0c5d2df115666e6942e94579b273</citedby><cites>FETCH-LOGICAL-c3664-6d539f3da34751979137d5345caf63c212ca0c5d2df115666e6942e94579b273</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmicr.20664$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmicr.20664$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19399878$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chaves, José C.</creatorcontrib><creatorcontrib>Fagundes, Djalma J.</creatorcontrib><creatorcontrib>Simões, Manuel De J.</creatorcontrib><creatorcontrib>Bertoletto, Paulo R.</creatorcontrib><creatorcontrib>Oshima, Celina T. F.</creatorcontrib><creatorcontrib>Taha, Murched O.</creatorcontrib><creatorcontrib>Simões, Ricardo S.</creatorcontrib><creatorcontrib>Fagundes, Anna L. N.</creatorcontrib><title>Hyperbaric oxygen therapy protects the liver from apoptosis caused by ischemia-reperfusion injury in rats</title><title>Microsurgery</title><addtitle>Microsurgery</addtitle><description>Purpose:
The present paper aimed to investigate the role of hyperbaric oxygen treatment (HBO) and the apoptosis in rat liver ischemia‐reperfusion injury (IRI).
Methods:
Thirty‐seven male Wistar rats were subjected to 30 minutes of hepatic ischemia and 30 minutes of reperfusion and randomly distributed into six groups: G‐I/R (n = 8), control without HBO; G‐HBO/I (n = 8), HBO only during the ischemia period; G‐HBO/R (n = 8), HBO only during the reperfusion period; G‐HBO‐I/R (n = 8), HBO during both the ischemia and reperfusion periods; G‐Sh (n = 3), HBO without ischemia or reperfusion as sham group; G‐C (n = 2) for control of current apoptosis expression on the normal liver tissue. HBO was carried out using a transparent, cylindrical acrylic chamber with a pressure of 2.0 ATA. Hepatic samples were stained for caspase‐3 cleavage.
Results:
Apoptotic cells were identified in all groups. In the hepatic specimens of animals HBO‐treated during ischemia (GHBO‐I), there was a significant decrease (P < 0.001) in the number of cells undergoing apoptosis (1.62 ± 0.91). The apoptotic index showed no significant difference in the animals HBO‐treated during ischemia/reperfusion (5.75 ± 1.28) compared with the G‐I/R (3.5 ± 0.75), which had no HBO treatment. The apoptosis index (11.25 ± 1.90) was significantly higher (P < 0.01) in HBO‐treated animals during the reperfusion period when compared with any of the other groups.
Conclusion:
A favorable effect was obtained when hyperbaric oxygen was administered early during ischemia. The hyperbaric oxygen in later periods of reperfusion was associated with a more severe apoptosis index. © 2009 Wiley‐Liss, Inc. Microsurgery 2009.</description><subject>Animals</subject><subject>Apoptosis - physiology</subject><subject>Caspase 3 - metabolism</subject><subject>Disease Models, Animal</subject><subject>Hyperbaric Oxygenation - methods</subject><subject>Immunohistochemistry</subject><subject>Liver - enzymology</subject><subject>Liver - physiopathology</subject><subject>Male</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Time Factors</subject><issn>0738-1085</issn><issn>1098-2752</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1O3DAUhS3UCgbohgdA3lWqFOqf2I6XdFQGBAWJjsTS8jg3YMhf7aSQt8fDDHTXlaXr73469yB0RMkJJYR9b7wLJ4xIme-gGSW6yJgS7BOaEcWLjJJC7KH9GB8JIVorvYv2qOZaF6qYIX8-9RBWNniHu5fpHlo8PECw_YT70A3ghrge4Nr_hYCr0DXY9l0_dNFH7OwYocSrCfvoHqDxNguQdNUYfddi3z6OIf21ONghHqLPla0jfNm-B2h59nM5P8-ubhYX89OrzPF0QSZLwXXFS8tzJWiKS7lKo1w4W0nuGGXOEidKVlaUCiklSJ0z0LlQesUUP0BfN9oU_88IcTBNCgd1bVvoxmgUz0lBtRCJ_LYhXehiDFCZPvjGhslQYtbFmnWx5q3YBB9vteOqgfIfum0yAXQDPPsapv-ozK-L-e27NNvs-DjAy8eODU9GKq6EubtemAVd_r7ML3-YO_4KmxaTyA</recordid><startdate>20090101</startdate><enddate>20090101</enddate><creator>Chaves, José C.</creator><creator>Fagundes, Djalma J.</creator><creator>Simões, Manuel De J.</creator><creator>Bertoletto, Paulo R.</creator><creator>Oshima, Celina T. F.</creator><creator>Taha, Murched O.</creator><creator>Simões, Ricardo S.</creator><creator>Fagundes, Anna L. N.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</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>20090101</creationdate><title>Hyperbaric oxygen therapy protects the liver from apoptosis caused by ischemia-reperfusion injury in rats</title><author>Chaves, José C. ; Fagundes, Djalma J. ; Simões, Manuel De J. ; Bertoletto, Paulo R. ; Oshima, Celina T. F. ; Taha, Murched O. ; Simões, Ricardo S. ; Fagundes, Anna L. N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3664-6d539f3da34751979137d5345caf63c212ca0c5d2df115666e6942e94579b273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Apoptosis - physiology</topic><topic>Caspase 3 - metabolism</topic><topic>Disease Models, Animal</topic><topic>Hyperbaric Oxygenation - methods</topic><topic>Immunohistochemistry</topic><topic>Liver - enzymology</topic><topic>Liver - physiopathology</topic><topic>Male</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chaves, José C.</creatorcontrib><creatorcontrib>Fagundes, Djalma J.</creatorcontrib><creatorcontrib>Simões, Manuel De J.</creatorcontrib><creatorcontrib>Bertoletto, Paulo R.</creatorcontrib><creatorcontrib>Oshima, Celina T. F.</creatorcontrib><creatorcontrib>Taha, Murched O.</creatorcontrib><creatorcontrib>Simões, Ricardo S.</creatorcontrib><creatorcontrib>Fagundes, Anna L. N.</creatorcontrib><collection>Istex</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>Microsurgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chaves, José C.</au><au>Fagundes, Djalma J.</au><au>Simões, Manuel De J.</au><au>Bertoletto, Paulo R.</au><au>Oshima, Celina T. F.</au><au>Taha, Murched O.</au><au>Simões, Ricardo S.</au><au>Fagundes, Anna L. N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperbaric oxygen therapy protects the liver from apoptosis caused by ischemia-reperfusion injury in rats</atitle><jtitle>Microsurgery</jtitle><addtitle>Microsurgery</addtitle><date>2009-01-01</date><risdate>2009</risdate><volume>29</volume><issue>7</issue><spage>578</spage><epage>583</epage><pages>578-583</pages><issn>0738-1085</issn><eissn>1098-2752</eissn><abstract>Purpose:
The present paper aimed to investigate the role of hyperbaric oxygen treatment (HBO) and the apoptosis in rat liver ischemia‐reperfusion injury (IRI).
Methods:
Thirty‐seven male Wistar rats were subjected to 30 minutes of hepatic ischemia and 30 minutes of reperfusion and randomly distributed into six groups: G‐I/R (n = 8), control without HBO; G‐HBO/I (n = 8), HBO only during the ischemia period; G‐HBO/R (n = 8), HBO only during the reperfusion period; G‐HBO‐I/R (n = 8), HBO during both the ischemia and reperfusion periods; G‐Sh (n = 3), HBO without ischemia or reperfusion as sham group; G‐C (n = 2) for control of current apoptosis expression on the normal liver tissue. HBO was carried out using a transparent, cylindrical acrylic chamber with a pressure of 2.0 ATA. Hepatic samples were stained for caspase‐3 cleavage.
Results:
Apoptotic cells were identified in all groups. In the hepatic specimens of animals HBO‐treated during ischemia (GHBO‐I), there was a significant decrease (P < 0.001) in the number of cells undergoing apoptosis (1.62 ± 0.91). The apoptotic index showed no significant difference in the animals HBO‐treated during ischemia/reperfusion (5.75 ± 1.28) compared with the G‐I/R (3.5 ± 0.75), which had no HBO treatment. The apoptosis index (11.25 ± 1.90) was significantly higher (P < 0.01) in HBO‐treated animals during the reperfusion period when compared with any of the other groups.
Conclusion:
A favorable effect was obtained when hyperbaric oxygen was administered early during ischemia. The hyperbaric oxygen in later periods of reperfusion was associated with a more severe apoptosis index. © 2009 Wiley‐Liss, Inc. Microsurgery 2009.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>19399878</pmid><doi>10.1002/micr.20664</doi><tpages>6</tpages></addata></record> |
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subjects | Animals Apoptosis - physiology Caspase 3 - metabolism Disease Models, Animal Hyperbaric Oxygenation - methods Immunohistochemistry Liver - enzymology Liver - physiopathology Male Rats Rats, Wistar Reperfusion Injury - physiopathology Reperfusion Injury - prevention & control Time Factors |
title | Hyperbaric oxygen therapy protects the liver from apoptosis caused by ischemia-reperfusion injury in rats |
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