GP IIb‐IIIa Receptor Blockers Minimize Vascular and Perivascular Damage in the Hippocampus after Cardiopulmonary Bypass Management
Identifieur interne : 001579 ( Istex/Corpus ); précédent : 001578; suivant : 001580GP IIb‐IIIa Receptor Blockers Minimize Vascular and Perivascular Damage in the Hippocampus after Cardiopulmonary Bypass Management
Auteurs : S. Arnhold ; H. Klein ; L. Benmime ; M. Südkamp ; K. AddicksSource :
- Anatomia, Histologia, Embryologia [ 0340-2096 ] ; 2005-12.
Abstract
Brain injury remains a significant and potentially devastating outcome of cardiopulmonary bypass (CPB) under circulatory arrest. These outcomes caused by a microvasculature embolization are associated with increased mortality, longer hospital stays and increased use of intermediate or long term care facilities. The administration of heparin in heart surgery during deep hypothermic cardiopulmonary bypass is the basic prophylactic strategy for reducing or even preventing, microvasculature embolization. Unfortunately, an incidence of neuropsychological impairments (NPI) is found in as many as 25 % of the survivors. As it is suspected that these impairments are correlated with morphological alterations, in our study we use the GP IIb‐IIIa receptor blocker Eptifibatide for the inhibition of platelet aggregation, in order to look for a reduction of tissue damage compared to the standard treatment. Two groups of 11 piglets (mean body weight of 15±5 kg) underwent 10‐minute normothermic bypass, 40‐minute cooling on cardiopulmonary bypass, 60‐minutes deep hypothermic circulatory arrest (DHCA) at 15°C, and 40‐minute rewarming to 37°C. Group 1 was treated only with unfractionated heparin (UFH), whereas Group 2 was medicated with Eptifibatide, in addition to the UFH‐treatment group 1. After rewarming, all animals underwent bilateral carotid perfusion with 4% paraformaldehyde. Histological investigations of semi thin sections reveal a marked decrease of hippocampal alterations by using the GP IIb‐IIIa receptor blocker in addition to standard UFH treatment. We detect a reduction of degenerative areas in perivascular (vessels with 10–30 μm in diameter) tissue. These semi‐quantitative data are confirmed by ultrastructural findings.
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DOI: 10.1111/j.1439-0264.2005.00669_11.x
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These outcomes caused by a microvasculature embolization are associated with increased mortality, longer hospital stays and increased use of intermediate or long term care facilities. The administration of heparin in heart surgery during deep hypothermic cardiopulmonary bypass is the basic prophylactic strategy for reducing or even preventing, microvasculature embolization. Unfortunately, an incidence of neuropsychological impairments (NPI) is found in as many as 25 % of the survivors. As it is suspected that these impairments are correlated with morphological alterations, in our study we use the GP IIb‐IIIa receptor blocker Eptifibatide for the inhibition of platelet aggregation, in order to look for a reduction of tissue damage compared to the standard treatment. Two groups of 11 piglets (mean body weight of 15±5 kg) underwent 10‐minute normothermic bypass, 40‐minute cooling on cardiopulmonary bypass, 60‐minutes deep hypothermic circulatory arrest (DHCA) at 15°C, and 40‐minute rewarming to 37°C. Group 1 was treated only with unfractionated heparin (UFH), whereas Group 2 was medicated with Eptifibatide, in addition to the UFH‐treatment group 1. After rewarming, all animals underwent bilateral carotid perfusion with 4% paraformaldehyde. Histological investigations of semi thin sections reveal a marked decrease of hippocampal alterations by using the GP IIb‐IIIa receptor blocker in addition to standard UFH treatment. We detect a reduction of degenerative areas in perivascular (vessels with 10–30 μm in diameter) tissue. These semi‐quantitative data are confirmed by ultrastructural findings.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>S. 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Two groups of 11 piglets (mean body weight of 15±5 kg) underwent 10‐minute normothermic bypass, 40‐minute cooling on cardiopulmonary bypass, 60‐minutes deep hypothermic circulatory arrest (DHCA) at 15°C, and 40‐minute rewarming to 37°C. Group 1 was treated only with unfractionated heparin (UFH), whereas Group 2 was medicated with Eptifibatide, in addition to the UFH‐treatment group 1. After rewarming, all animals underwent bilateral carotid perfusion with 4% paraformaldehyde. Histological investigations of semi thin sections reveal a marked decrease of hippocampal alterations by using the GP IIb‐IIIa receptor blocker in addition to standard UFH treatment. We detect a reduction of degenerative areas in perivascular (vessels with 10–30 μm in diameter) tissue. 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Two groups of 11 piglets (mean body weight of 15±5 kg) underwent 10‐minute normothermic bypass, 40‐minute cooling on cardiopulmonary bypass, 60‐minutes deep hypothermic circulatory arrest (DHCA) at 15°C, and 40‐minute rewarming to 37°C. Group 1 was treated only with unfractionated heparin (UFH), whereas Group 2 was medicated with Eptifibatide, in addition to the UFH‐treatment group 1. After rewarming, all animals underwent bilateral carotid perfusion with 4% paraformaldehyde. Histological investigations of semi thin sections reveal a marked decrease of hippocampal alterations by using the GP IIb‐IIIa receptor blocker in addition to standard UFH treatment. We detect a reduction of degenerative areas in perivascular (vessels with 10–30 μm in diameter) tissue. These semi‐quantitative data are confirmed by ultrastructural findings.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>GP IIb‐IIIa Receptor Blockers Minimize Vascular and Perivascular Damage in the Hippocampus after Cardiopulmonary Bypass Management</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Abstracts</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>GP IIb‐IIIa Receptor Blockers Minimize Vascular and Perivascular Damage in the Hippocampus after Cardiopulmonary Bypass Management</title></titleInfo><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Arnhold</namePart><affiliation>Department of Anatomy I, University of Cologne, J.‐Stelzmanstrasse 9, 50931 Köln, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Klein</namePart><affiliation>Department of Anatomy I, University of Cologne, J.‐Stelzmanstrasse 9, 50931 Köln, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">BenMime</namePart><affiliation>Clinic for Cardiosurgery, University of Cologne, J.‐Stelzmanstrasse 9, 50931 Köln, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Südkamp</namePart><affiliation>Clinic for Cardiosurgery, University of Cologne, J.‐Stelzmanstrasse 9, 50931 Köln, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Addicks</namePart><affiliation>Department of Anatomy I, University of Cologne, J.‐Stelzmanstrasse 9, 50931 Köln, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="abstract" displayLabel="abstract"></genre><originInfo><publisher>Blackwell Verlag GmbH</publisher><place><placeTerm type="text">Berlin, Germany</placeTerm></place><dateIssued encoding="w3cdtf">2005-12</dateIssued><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Brain injury remains a significant and potentially devastating outcome of cardiopulmonary bypass (CPB) under circulatory arrest. These outcomes caused by a microvasculature embolization are associated with increased mortality, longer hospital stays and increased use of intermediate or long term care facilities. The administration of heparin in heart surgery during deep hypothermic cardiopulmonary bypass is the basic prophylactic strategy for reducing or even preventing, microvasculature embolization. Unfortunately, an incidence of neuropsychological impairments (NPI) is found in as many as 25 % of the survivors. As it is suspected that these impairments are correlated with morphological alterations, in our study we use the GP IIb‐IIIa receptor blocker Eptifibatide for the inhibition of platelet aggregation, in order to look for a reduction of tissue damage compared to the standard treatment. Two groups of 11 piglets (mean body weight of 15±5 kg) underwent 10‐minute normothermic bypass, 40‐minute cooling on cardiopulmonary bypass, 60‐minutes deep hypothermic circulatory arrest (DHCA) at 15°C, and 40‐minute rewarming to 37°C. Group 1 was treated only with unfractionated heparin (UFH), whereas Group 2 was medicated with Eptifibatide, in addition to the UFH‐treatment group 1. After rewarming, all animals underwent bilateral carotid perfusion with 4% paraformaldehyde. Histological investigations of semi thin sections reveal a marked decrease of hippocampal alterations by using the GP IIb‐IIIa receptor blocker in addition to standard UFH treatment. We detect a reduction of degenerative areas in perivascular (vessels with 10–30 μm in diameter) tissue. These semi‐quantitative data are confirmed by ultrastructural findings.</abstract><relatedItem type="host"><titleInfo><title>Anatomia, Histologia, Embryologia</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0340-2096</identifier><identifier type="eISSN">1439-0264</identifier><identifier type="DOI">10.1111/(ISSN)1439-0264</identifier><identifier type="PublisherID">AHE</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>34</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>s1</number></detail><extent unit="pages"><start>5</start><end>5</end></extent></part></relatedItem><identifier type="istex">5F028A045A81AC1483A5CC5D5A27D75F44759532</identifier><identifier type="DOI">10.1111/j.1439-0264.2005.00669_11.x</identifier><identifier type="ArticleID">AHE669_11_11</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Verlag GmbH</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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