Transcapillary exchange of indium 111-labeled anticardiac myosin Fab and thallium 201 in isolated reperfused rabbit hearts
Identifieur interne : 000142 ( Main/Exploration ); précédent : 000141; suivant : 000143Transcapillary exchange of indium 111-labeled anticardiac myosin Fab and thallium 201 in isolated reperfused rabbit hearts
Auteurs : RBID : ISTEX:12350_1994_Article_BF02940337.pdfEnglish descriptors
Abstract
BackgroundThe physiologic mechanisms of111In-labeled anticardiac myosin antibody [111In]-AM) imaging are fairly well established. However, to better understand the transcapillary exchange characteristics of normal and reperfused myocardium, a standard first-pass, indicator-dilution analysis was undertaken in hearts subjected to global no-flow and low-flow ischemia.Methods and ResultsThe first-pass myocardial transport of201Tl and [111In]-AM was evaluated in an in vitro rabbit model of no-flow ischemia/reperfusion with indicator-dilution analysis during normal and ischemic flows and whole-blood perfusate. The maximum extraction fraction (Emax) of201Tl was dominated by flow rate as expected and averaged 0.75 (±0.009) and 0.57 (±0.008) during ischemic and normal flows, respectively (p<0.01). Emax values for [111In]-AM, which were 0.02 or less in all hearts at control, increased to 0.06 or greater at moderate to longer perfusion times after 50 or more minutes of no-flow ischemia. Permeability surface area (in milliliters per minute per gram) tended to decline for201Tl with longer reperfusion periods in both ischemic and normal flow groups and paralleled the changes observed for Emax for [111In]-AM.ConclusionsThese data demonstrate that the first-pass extraction of [111In]-AM is quite low in this model of acute coronary occlusion and reflow and enhanced only in severe ischemia-reperfusion treatment. Therefore in this model there appears to be no significant [111In]-AM uptake in either normal or mildly ischemic myocardium. Consequently, [111In]-AM uptake into myocardium must depend on tracer recirculation, as well as sarcolemmal cell wall disruption, to achieve specific and sufficient [111In]-AM uptake for localization of clinical imaging.
DOI: 10.1007/BF02940337
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<record><TEI><teiHeader><fileDesc><titleStmt><title>Transcapillary exchange of indium 111-labeled anticardiac myosin Fab and thallium 201 in isolated reperfused rabbit hearts</title><author><name>Denis J. Meerdink</name><affiliation><mods:affiliation>From the Department of Physiology and Pharmacology, Myocardial Research Laboratory, School of Pharmacy, University of the Pacific, 95211, Stockton, CA, </mods:affiliation><wicri:noCountry code="subField"></wicri:noCountry></affiliation><affiliation><mods:affiliation>the Departments of Nuclear Medicine and Medicine, Division of Cardiology, Myocardial Isotope Research Laboratory, University of Massachusetts Medical Center, Worcester, Mass., </mods:affiliation><wicri:noCountry code="subField"></wicri:noCountry></affiliation></author><author><name>Jeffrey A. Leppo</name><affiliation><mods:affiliation>From the Department of Physiology and Pharmacology, Myocardial Research Laboratory, School of Pharmacy, University of the Pacific, 95211, Stockton, CA, </mods:affiliation><wicri:noCountry code="subField"></wicri:noCountry></affiliation><affiliation><mods:affiliation>the Departments of Nuclear Medicine and Medicine, Division of Cardiology, Myocardial Isotope Research Laboratory, University of Massachusetts Medical Center, Worcester, Mass., </mods:affiliation><wicri:noCountry code="subField"></wicri:noCountry></affiliation></author></titleStmt><publicationStmt><idno type="RBID">ISTEX:12350_1994_Article_BF02940337.pdf</idno><date when="1994">1994</date><idno type="doi">10.1007/BF02940337</idno><idno type="wicri:Area/Main/Corpus">000C98</idno><idno type="wicri:Area/Main/Curation">000C98</idno><idno type="wicri:Area/Main/Exploration">000142</idno></publicationStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antimyosin</term><term>First-pass extraction</term><term>Indicator dilution</term><term>Isolated rabbit heart</term><term>Reperfusion</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="eng">BackgroundThe physiologic mechanisms of111In-labeled anticardiac myosin antibody [111In]-AM) imaging are fairly well established. However, to better understand the transcapillary exchange characteristics of normal and reperfused myocardium, a standard first-pass, indicator-dilution analysis was undertaken in hearts subjected to global no-flow and low-flow ischemia.Methods and ResultsThe first-pass myocardial transport of201Tl and [111In]-AM was evaluated in an in vitro rabbit model of no-flow ischemia/reperfusion with indicator-dilution analysis during normal and ischemic flows and whole-blood perfusate. The maximum extraction fraction (Emax) of201Tl was dominated by flow rate as expected and averaged 0.75 (±0.009) and 0.57 (±0.008) during ischemic and normal flows, respectively (p<0.01). Emax values for [111In]-AM, which were 0.02 or less in all hearts at control, increased to 0.06 or greater at moderate to longer perfusion times after 50 or more minutes of no-flow ischemia. Permeability surface area (in milliliters per minute per gram) tended to decline for201Tl with longer reperfusion periods in both ischemic and normal flow groups and paralleled the changes observed for Emax for [111In]-AM.ConclusionsThese data demonstrate that the first-pass extraction of [111In]-AM is quite low in this model of acute coronary occlusion and reflow and enhanced only in severe ischemia-reperfusion treatment. Therefore in this model there appears to be no significant [111In]-AM uptake in either normal or mildly ischemic myocardium. Consequently, [111In]-AM uptake into myocardium must depend on tracer recirculation, as well as sarcolemmal cell wall disruption, to achieve specific and sufficient [111In]-AM uptake for localization of clinical imaging.</div></front></TEI><mods xsi:schemaLocation="http://www.loc.gov/mods/v3 file:///applis/istex/home/loadistex/home/etc/xsd/mods.xsd" version="3.4" istexId="e0e2ac53cfd8d748f6079e75bf5db88d66a1fdba"><titleInfo lang="eng"><title>Transcapillary exchange of indium 111-labeled anticardiac myosin Fab and thallium 201 in isolated reperfused rabbit hearts</title></titleInfo><name type="personal"><namePart type="given">Denis J.</namePart><namePart type="family">Meerdink</namePart><namePart type="termsOfAddress">PhD</namePart><role><roleTerm type="text">author</roleTerm></role><affiliation>From the Department of Physiology and Pharmacology, Myocardial Research Laboratory, School of Pharmacy, University of the Pacific, 95211, Stockton, CA, </affiliation><affiliation>the Departments of Nuclear Medicine and Medicine, Division of Cardiology, Myocardial Isotope Research Laboratory, University of Massachusetts Medical Center, Worcester, Mass., </affiliation></name><name type="personal"><namePart type="given">Jeffrey A.</namePart><namePart type="family">Leppo</namePart><namePart type="termsOfAddress">MD</namePart><role><roleTerm type="text">author</roleTerm></role><affiliation>From the Department of Physiology and Pharmacology, Myocardial Research Laboratory, School of Pharmacy, University of the Pacific, 95211, Stockton, CA, </affiliation><affiliation>the Departments of Nuclear Medicine and Medicine, Division of Cardiology, Myocardial Isotope Research Laboratory, University of Massachusetts Medical Center, Worcester, Mass., </affiliation></name><typeOfResource>text</typeOfResource><genre>Original Articles</genre><genre>Original Paper</genre><originInfo><publisher>Springer-Verlag, New York</publisher><dateCreated encoding="w3cdtf">1993-11-05</dateCreated><dateCaptured encoding="w3cdtf">1994-01-18</dateCaptured><dateValid encoding="w3cdtf">2008-08-27</dateValid><copyrightDate encoding="w3cdtf">1994</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="eng">BackgroundThe physiologic mechanisms of111In-labeled anticardiac myosin antibody [111In]-AM) imaging are fairly well established. However, to better understand the transcapillary exchange characteristics of normal and reperfused myocardium, a standard first-pass, indicator-dilution analysis was undertaken in hearts subjected to global no-flow and low-flow ischemia.Methods and ResultsThe first-pass myocardial transport of201Tl and [111In]-AM was evaluated in an in vitro rabbit model of no-flow ischemia/reperfusion with indicator-dilution analysis during normal and ischemic flows and whole-blood perfusate. The maximum extraction fraction (Emax) of201Tl was dominated by flow rate as expected and averaged 0.75 (±0.009) and 0.57 (±0.008) during ischemic and normal flows, respectively (p<0.01). Emax values for [111In]-AM, which were 0.02 or less in all hearts at control, increased to 0.06 or greater at moderate to longer perfusion times after 50 or more minutes of no-flow ischemia. Permeability surface area (in milliliters per minute per gram) tended to decline for201Tl with longer reperfusion periods in both ischemic and normal flow groups and paralleled the changes observed for Emax for [111In]-AM.ConclusionsThese data demonstrate that the first-pass extraction of [111In]-AM is quite low in this model of acute coronary occlusion and reflow and enhanced only in severe ischemia-reperfusion treatment. Therefore in this model there appears to be no significant [111In]-AM uptake in either normal or mildly ischemic myocardium. Consequently, [111In]-AM uptake into myocardium must depend on tracer recirculation, as well as sarcolemmal cell wall disruption, to achieve specific and sufficient [111In]-AM uptake for localization of clinical imaging.</abstract><subject lang="eng"><genre>Key Words</genre><topic>antimyosin</topic><topic>reperfusion</topic><topic>indicator dilution</topic><topic>first-pass extraction</topic><topic>isolated rabbit heart</topic></subject><relatedItem type="series"><titleInfo type="abbreviated"><title>J. Nucl. Cardiol.</title></titleInfo><titleInfo><title>Journal of Nuclear Cardiology</title><partNumber>Year: 1994</partNumber><partNumber>Volume: 1</partNumber><partNumber>Number: 3</partNumber></titleInfo><genre>Archive Journal</genre><originInfo><dateIssued encoding="w3cdtf">1994-05-01</dateIssued><copyrightDate encoding="w3cdtf">1994</copyrightDate></originInfo><subject usage="primary"><topic>Medicine & Public Health</topic><topic>Nuclear Medicine</topic><topic>Cardiology</topic><topic>Imaging / Radiology</topic></subject><identifier type="issn">1071-3581</identifier><identifier type="issn">Electronic: 1532-6551</identifier><identifier type="matrixNumber">12350</identifier><identifier type="local">IssueArticleCount: 12</identifier><recordInfo><recordOrigin>American Society of Nuclear Cardiology, 1994</recordOrigin></recordInfo></relatedItem><identifier type="doi">10.1007/BF02940337</identifier><identifier type="matrixNumber">Art3</identifier><identifier type="local">BF02940337</identifier><accessCondition type="use and reproduction">MetadataGrant: OpenAccess</accessCondition><accessCondition type="use and reproduction">AbstractGrant: OpenAccess</accessCondition><accessCondition type="restriction on access">BodyPDFGrant: Restricted</accessCondition><accessCondition type="restriction on access">BodyHTMLGrant: Restricted</accessCondition><accessCondition type="restriction on access">BibliographyGrant: Restricted</accessCondition><accessCondition type="restriction on access">ESMGrant: Restricted</accessCondition><part><extent unit="pages"><start>236</start><end>245</end></extent></part><recordInfo><recordOrigin>American Society of Nuclear Cardiology, 1994</recordOrigin><recordIdentifier>12350_1994_Article_BF02940337.pdf</recordIdentifier></recordInfo></mods></record>Pour manipuler ce document sous Unix (Dilib)
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