Evaluation of Multiple-Quantum-Filtered23Na NMR in Monitoring Intracellular Na Content in the Isolated Perfused Rat Heart in the Absence of a Chemical-Shift Reagent
Identifieur interne : 000D06 ( Istex/Corpus ); précédent : 000D05; suivant : 000D07Evaluation of Multiple-Quantum-Filtered23Na NMR in Monitoring Intracellular Na Content in the Isolated Perfused Rat Heart in the Absence of a Chemical-Shift Reagent
Auteurs : Joseph S. Tauskela ; José M. Dizon ; John Whang ; José KatzSource :
- Journal of Magnetic Resonance [ 1090-7807 ] ; 1997.
English descriptors
- KwdEn :
- Amplitude, Atpase inhibitor, Baseline, Biophys, Cell volume, Creation time, Current study, Data points, Ddqftotal, Destructive interference, Direct comparison, Dqfex, Dqfex spectra, Dqftotal, Dqftotal spectrum, Dsqin, Dtqfin, Dtqftotal, Extracellular, Extracellular spectra, Gdb0t, Identical estimates, Intracellular, Intracellular volume, Ischemia, Maga, Maga sodium spectra, Magn, Magnetization, Monitoring nain content, Naex, Nain, Nain content, Navon, Normal baseline conditions, Normal baseline levels, Ouabain, Perfusate, Perfused, Perfusion, Preischemic, Preischemic levels, Pulse sequence, Reagent, Relaxation behavior, Reson, Spectrum, Sqin, Sqin spectra, Tauskela, Tensor, Tmax, Tqfex, Tqfex spectra, Tqfin, Tqfin spectra, Tqfin spectrum, Tqftotal, Transverse relaxation behavior, Transverse relaxation times.
- Teeft :
- Amplitude, Atpase inhibitor, Baseline, Biophys, Cell volume, Creation time, Current study, Data points, Ddqftotal, Destructive interference, Direct comparison, Dqfex, Dqfex spectra, Dqftotal, Dqftotal spectrum, Dsqin, Dtqfin, Dtqftotal, Extracellular, Extracellular spectra, Gdb0t, Identical estimates, Intracellular, Intracellular volume, Ischemia, Maga, Maga sodium spectra, Magn, Magnetization, Monitoring nain content, Naex, Nain, Nain content, Navon, Normal baseline conditions, Normal baseline levels, Ouabain, Perfusate, Perfused, Perfusion, Preischemic, Preischemic levels, Pulse sequence, Reagent, Relaxation behavior, Reson, Spectrum, Sqin, Sqin spectra, Tauskela, Tensor, Tmax, Tqfex, Tqfex spectra, Tqfin, Tqfin spectra, Tqfin spectrum, Tqftotal, Transverse relaxation behavior, Transverse relaxation times.
Abstract
Abstract: The feasibility of employing triple-quantum-filtered (TQF) or double-quantum-filtered (DQF)23Na NMR spectra to monitor intracellular Na (Nain) content in isolated rat hearts perfused in the absence of a chemical-shift reagent (SR) was investigated. This necessitated characterization of the following: first, the pool of Nainrepresented by the intracellular TQF (TQFin) spectrum; second, the maximum extent to which altered transverse relaxation times affect TQFinspectral amplitudes; and finally, the situations for which the SR-free method can reliably be applied. The rates of increase in peak amplitudes of both intracellular TQF spectra, adjusted for changes in both fast (T2f) and slow (T2s) transverse relaxation times, and intracellular single-quantum (SQin) spectra were identical during no-flow ischemia, indicating that TQFinand SQinspectra represent the same Nainpopulation. Addition of an Na/K ATPase inhibitor, ouabain (≥500 μM), and no-flow ischemia induced similar rates of increase of Naincontent. However, the Nainlevel for which theT2values started to increase was lower for ischemic (<140% of preischemic values) than for ouabain-exposed (>165%) hearts, which is consistent with the known earlier onset of intracellular swelling in ischemic hearts. Exposure of hearts to hyperosmotic perfusate (200 mMsucrose) increased [Nain], due to a decreased cell volume and an unchanged Naincontent, but caused a decrease inT2values, a trend opposite to that observed with exposure of hearts to ouabain or ischemia.T2values therefore consistently correlated only with cell volume, not with Naincontent or concentration, indicating an important role for intracellular macromolecule concentration in modulating transverse relaxation behavior. The combined effect of ischemia-induced increases inT2values and their inhomogeneous broadened forms was an ∼6% overestimation of Naincontent from amplitudes of SR-aided TQFinspectra, indicating negligible effect of transverse relaxation-dependent alterations on TQFinspectral amplitudes. Thus, Naincontent may be reliably determined from SR-free TQF spectra when the contribution from extracellular Na does not appreciably vary, such as during constant pressure perfusion. Following complete reduction in perfusion pressure, both SR-free TQF and DQF spectra respond to increases in Naincontent. However, SR-free DQF NMR provides an estimate of Naincontent much closer to that provided by the SR-aided method, due to the appreciable decrease of the extracellular DQF signal resulting from destructive interference between second- and third-rank tensors.
Url:
DOI: 10.1006/jmre.1997.1181
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ISTEX:3C05A9E93E0F1B48AB7295845D12804B6E2E007DLe document en format XML
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This necessitated characterization of the following: first, the pool of Nainrepresented by the intracellular TQF (TQFin) spectrum; second, the maximum extent to which altered transverse relaxation times affect TQFinspectral amplitudes; and finally, the situations for which the SR-free method can reliably be applied. The rates of increase in peak amplitudes of both intracellular TQF spectra, adjusted for changes in both fast (T2f) and slow (T2s) transverse relaxation times, and intracellular single-quantum (SQin) spectra were identical during no-flow ischemia, indicating that TQFinand SQinspectra represent the same Nainpopulation. Addition of an Na/K ATPase inhibitor, ouabain (≥500 μM), and no-flow ischemia induced similar rates of increase of Naincontent. However, the Nainlevel for which theT2values started to increase was lower for ischemic (<140% of preischemic values) than for ouabain-exposed (>165%) hearts, which is consistent with the known earlier onset of intracellular swelling in ischemic hearts. Exposure of hearts to hyperosmotic perfusate (200 mMsucrose) increased [Nain], due to a decreased cell volume and an unchanged Naincontent, but caused a decrease inT2values, a trend opposite to that observed with exposure of hearts to ouabain or ischemia.T2values therefore consistently correlated only with cell volume, not with Naincontent or concentration, indicating an important role for intracellular macromolecule concentration in modulating transverse relaxation behavior. The combined effect of ischemia-induced increases inT2values and their inhomogeneous broadened forms was an ∼6% overestimation of Naincontent from amplitudes of SR-aided TQFinspectra, indicating negligible effect of transverse relaxation-dependent alterations on TQFinspectral amplitudes. Thus, Naincontent may be reliably determined from SR-free TQF spectra when the contribution from extracellular Na does not appreciably vary, such as during constant pressure perfusion. Following complete reduction in perfusion pressure, both SR-free TQF and DQF spectra respond to increases in Naincontent. However, SR-free DQF NMR provides an estimate of Naincontent much closer to that provided by the SR-aided method, due to the appreciable decrease of the extracellular DQF signal resulting from destructive interference between second- and third-rank tensors.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>nain</json:string><json:string>ischemia</json:string><json:string>nain content</json:string><json:string>tqfin</json:string><json:string>intracellular</json:string><json:string>extracellular</json:string><json:string>dtqfin</json:string><json:string>sqin</json:string><json:string>dsqin</json:string><json:string>ouabain</json:string><json:string>tensor</json:string><json:string>sqin spectra</json:string><json:string>tmax</json:string><json:string>naex</json:string><json:string>dqfex</json:string><json:string>tqftotal</json:string><json:string>perfusate</json:string><json:string>dqftotal</json:string><json:string>tqfex</json:string><json:string>tqfin spectra</json:string><json:string>cell volume</json:string><json:string>dtqftotal</json:string><json:string>magn</json:string><json:string>transverse relaxation times</json:string><json:string>reson</json:string><json:string>maga</json:string><json:string>preischemic</json:string><json:string>ddqftotal</json:string><json:string>current study</json:string><json:string>tauskela</json:string><json:string>monitoring nain content</json:string><json:string>baseline</json:string><json:string>perfused</json:string><json:string>navon</json:string><json:string>magnetization</json:string><json:string>perfusion</json:string><json:string>transverse relaxation behavior</json:string><json:string>gdb0t</json:string><json:string>biophys</json:string><json:string>creation time</json:string><json:string>dqfex spectra</json:string><json:string>spectrum</json:string><json:string>amplitude</json:string><json:string>destructive interference</json:string><json:string>normal baseline conditions</json:string><json:string>pulse sequence</json:string><json:string>extracellular spectra</json:string><json:string>data points</json:string><json:string>dqftotal spectrum</json:string><json:string>preischemic levels</json:string><json:string>direct comparison</json:string><json:string>tqfex spectra</json:string><json:string>intracellular volume</json:string><json:string>normal baseline levels</json:string><json:string>tqfin spectrum</json:string><json:string>atpase inhibitor</json:string><json:string>relaxation behavior</json:string><json:string>identical estimates</json:string><json:string>maga sodium spectra</json:string><json:string>reagent</json:string></teeft></keywords><author><json:item><name>Joseph S. Tauskela</name><affiliations><json:string>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</json:string></affiliations></json:item><json:item><name>José M. Dizon</name><affiliations><json:string>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</json:string></affiliations></json:item><json:item><name>John Whang</name><affiliations><json:string>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</json:string></affiliations></json:item><json:item><name>José Katz</name><affiliations><json:string>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</json:string></affiliations></json:item></author><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>The feasibility of employing triple-quantum-filtered (TQF) or double-quantum-filtered (DQF)23Na NMR spectra to monitor intracellular Na (Nain) content in isolated rat hearts perfused in the absence of a chemical-shift reagent (SR) was investigated. This necessitated characterization of the following: first, the pool of Nainrepresented by the intracellular TQF (TQFin) spectrum; second, the maximum extent to which altered transverse relaxation times affect TQFinspectral amplitudes; and finally, the situations for which the SR-free method can reliably be applied. The rates of increase in peak amplitudes of both intracellular TQF spectra, adjusted for changes in both fast (T2f) and slow (T2s) transverse relaxation times, and intracellular single-quantum (SQin) spectra were identical during no-flow ischemia, indicating that TQFinand SQinspectra represent the same Nainpopulation. Addition of an Na/K ATPase inhibitor, ouabain (≥500 μM), and no-flow ischemia induced similar rates of increase of Naincontent. However, the Nainlevel for which theT2values started to increase was lower for ischemic (>140% of preischemic values) than for ouabain-exposed (>165%) hearts, which is consistent with the known earlier onset of intracellular swelling in ischemic hearts. Exposure of hearts to hyperosmotic perfusate (200 mMsucrose) increased [Nain], due to a decreased cell volume and an unchanged Naincontent, but caused a decrease inT2values, a trend opposite to that observed with exposure of hearts to ouabain or ischemia.T2values therefore consistently correlated only with cell volume, not with Naincontent or concentration, indicating an important role for intracellular macromolecule concentration in modulating transverse relaxation behavior. The combined effect of ischemia-induced increases inT2values and their inhomogeneous broadened forms was an ∼6% overestimation of Naincontent from amplitudes of SR-aided TQFinspectra, indicating negligible effect of transverse relaxation-dependent alterations on TQFinspectral amplitudes. Thus, Naincontent may be reliably determined from SR-free TQF spectra when the contribution from extracellular Na does not appreciably vary, such as during constant pressure perfusion. Following complete reduction in perfusion pressure, both SR-free TQF and DQF spectra respond to increases in Naincontent. However, SR-free DQF NMR provides an estimate of Naincontent much closer to that provided by the SR-aided method, due to the appreciable decrease of the extracellular DQF signal resulting from destructive interference between second- and third-rank tensors.</abstract><qualityIndicators><score>8</score><pdfVersion>1.1</pdfVersion><pdfPageSize>540 x 720 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>2603</abstractCharCount><pdfWordCount>9451</pdfWordCount><pdfCharCount>51868</pdfCharCount><pdfPageCount>13</pdfPageCount><abstractWordCount>350</abstractWordCount></qualityIndicators><title>Evaluation of Multiple-Quantum-Filtered23Na NMR in Monitoring Intracellular Na Content in the Isolated Perfused Rat Heart in the Absence of a Chemical-Shift Reagent</title><pii><json:string>S1090-7807(97)91181-2</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Journal of Magnetic Resonance</title><language><json:string>unknown</json:string></language><publicationDate>1997</publicationDate><issn><json:string>1090-7807</json:string></issn><pii><json:string>S1090-7807(00)X0060-2</json:string></pii><volume>127</volume><issue>1</issue><pages><first>115</first><last>127</last></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>spectroscopy</json:string><json:string>physics, atomic, molecular & chemical</json:string><json:string>biochemical research methods</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>biomedical research</json:string><json:string>biophysics</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences biologiques fondamentales et appliquees. psychologie</json:string><json:string>vertebres: systeme cardiovasculaire</json:string></inist></categories><publicationDate>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1006/jmre.1997.1181</json:string></doi><id>3C05A9E93E0F1B48AB7295845D12804B6E2E007D</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/3C05A9E93E0F1B48AB7295845D12804B6E2E007D/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/3C05A9E93E0F1B48AB7295845D12804B6E2E007D/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/3C05A9E93E0F1B48AB7295845D12804B6E2E007D/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Evaluation of Multiple-Quantum-Filtered23Na NMR in Monitoring Intracellular Na Content in the Isolated Perfused Rat Heart in the Absence of a Chemical-Shift Reagent</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>©1997 Academic Press</p></availability><date>1997</date></publicationStmt><notesStmt><note type="content">Section title: Regular Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Evaluation of Multiple-Quantum-Filtered23Na NMR in Monitoring Intracellular Na Content in the Isolated Perfused Rat Heart in the Absence of a Chemical-Shift Reagent</title><author xml:id="author-0000"><persName><forename type="first">Joseph S.</forename><surname>Tauskela</surname></persName><note type="biography">Present address: National Research Council, Institute for Biological Sciences, Building M-54, Montreal Road Campus, Ottawa, Ontario, Canada K1A 0R6.</note><affiliation>Present address: National Research Council, Institute for Biological Sciences, Building M-54, Montreal Road Campus, Ottawa, Ontario, Canada K1A 0R6.</affiliation><affiliation>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</affiliation></author><author xml:id="author-0001"><persName><forename type="first">José M.</forename><surname>Dizon</surname></persName><affiliation>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</affiliation></author><author xml:id="author-0002"><persName><forename type="first">John</forename><surname>Whang</surname></persName><affiliation>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</affiliation></author><author xml:id="author-0003"><persName><forename type="first">José</forename><surname>Katz</surname></persName><affiliation>To whom correspondence should be addressed: Department of Medicine, Division of Cardiology, Columbia University, PH 10-Stem, 630 West 168th Street, New York, NY 10032.</affiliation><affiliation>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</affiliation></author><idno type="istex">3C05A9E93E0F1B48AB7295845D12804B6E2E007D</idno><idno type="DOI">10.1006/jmre.1997.1181</idno><idno type="PII">S1090-7807(97)91181-2</idno></analytic><monogr><title level="j">Journal of Magnetic Resonance</title><title level="j" type="abbrev">YJMRE</title><idno type="pISSN">1090-7807</idno><idno type="PII">S1090-7807(00)X0060-2</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1997"></date><biblScope unit="volume">127</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="115">115</biblScope><biblScope unit="page" to="127">127</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The feasibility of employing triple-quantum-filtered (TQF) or double-quantum-filtered (DQF)23Na NMR spectra to monitor intracellular Na (Nain) content in isolated rat hearts perfused in the absence of a chemical-shift reagent (SR) was investigated. This necessitated characterization of the following: first, the pool of Nainrepresented by the intracellular TQF (TQFin) spectrum; second, the maximum extent to which altered transverse relaxation times affect TQFinspectral amplitudes; and finally, the situations for which the SR-free method can reliably be applied. The rates of increase in peak amplitudes of both intracellular TQF spectra, adjusted for changes in both fast (T2f) and slow (T2s) transverse relaxation times, and intracellular single-quantum (SQin) spectra were identical during no-flow ischemia, indicating that TQFinand SQinspectra represent the same Nainpopulation. Addition of an Na/K ATPase inhibitor, ouabain (≥500 μM), and no-flow ischemia induced similar rates of increase of Naincontent. However, the Nainlevel for which theT2values started to increase was lower for ischemic (<140% of preischemic values) than for ouabain-exposed (>165%) hearts, which is consistent with the known earlier onset of intracellular swelling in ischemic hearts. Exposure of hearts to hyperosmotic perfusate (200 mMsucrose) increased [Nain], due to a decreased cell volume and an unchanged Naincontent, but caused a decrease inT2values, a trend opposite to that observed with exposure of hearts to ouabain or ischemia.T2values therefore consistently correlated only with cell volume, not with Naincontent or concentration, indicating an important role for intracellular macromolecule concentration in modulating transverse relaxation behavior. The combined effect of ischemia-induced increases inT2values and their inhomogeneous broadened forms was an ∼6% overestimation of Naincontent from amplitudes of SR-aided TQFinspectra, indicating negligible effect of transverse relaxation-dependent alterations on TQFinspectral amplitudes. Thus, Naincontent may be reliably determined from SR-free TQF spectra when the contribution from extracellular Na does not appreciably vary, such as during constant pressure perfusion. Following complete reduction in perfusion pressure, both SR-free TQF and DQF spectra respond to increases in Naincontent. However, SR-free DQF NMR provides an estimate of Naincontent much closer to that provided by the SR-aided method, due to the appreciable decrease of the extracellular DQF signal resulting from destructive interference between second- and third-rank tensors.</p></abstract></profileDesc><revisionDesc><change when="1997-04-10">Modified</change><change when="1997">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/3C05A9E93E0F1B48AB7295845D12804B6E2E007D/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>YJMRE</jid><aid>91181</aid><ce:pii>S1090-7807(97)91181-2</ce:pii><ce:doi>10.1006/jmre.1997.1181</ce:doi><ce:copyright type="full-transfer" year="1997">Academic Press</ce:copyright></item-info><head><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title>Evaluation of Multiple-Quantum-Filtered<ce:sup>23</ce:sup>Na NMR in Monitoring Intracellular Na Content in the Isolated Perfused Rat Heart in the Absence of a Chemical-Shift Reagent</ce:title><ce:author-group><ce:author><ce:given-name>Joseph S.</ce:given-name><ce:surname>Tauskela</ce:surname><ce:cross-ref refid="MN971181A1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="MN971181FNDAG">†<ce:footnote id="MN971181FNDAG"><ce:label>†</ce:label><ce:note-para>Present address: National Research Council, Institute for Biological Sciences, Building M-54, Montreal Road Campus, Ottawa, Ontario, Canada K1A 0R6.</ce:note-para></ce:footnote></ce:cross-ref></ce:author><ce:author><ce:given-name>José M.</ce:given-name><ce:surname>Dizon</ce:surname><ce:cross-ref refid="MN971181A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>John</ce:given-name><ce:surname>Whang</ce:surname><ce:cross-ref refid="MN971181A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>José</ce:given-name><ce:surname>Katz</ce:surname><ce:cross-ref refid="MN971181A1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="MN971181A3"><ce:sup>b</ce:sup></ce:cross-ref><ce:cross-ref refid="MN971181FNSEC">§<ce:footnote id="MN971181FNSEC"><ce:label>§</ce:label><ce:note-para>To whom correspondence should be addressed: Department of Medicine, Division of Cardiology, Columbia University, PH 10-Stem, 630 West 168th Street, New York, NY 10032.</ce:note-para></ce:footnote></ce:cross-ref></ce:author><ce:affiliation id="MN971181A1"><ce:label>a</ce:label><ce:textfn>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</ce:textfn></ce:affiliation><ce:affiliation id="MN971181A3"><ce:label>b</ce:label><ce:textfn>Division of Cardiology, Department of Radiology, College of Physicians & Surgeons, Columbia University, New York, New York</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="23" month="12" year="1996"></ce:date-received><ce:date-revised day="10" month="4" year="1997"></ce:date-revised><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The feasibility of employing triple-quantum-filtered (TQF) or double-quantum-filtered (DQF)<ce:sup>23</ce:sup>Na NMR spectra to monitor intracellular Na (Na<ce:inf>in</ce:inf>) content in isolated rat hearts perfused in the absence of a chemical-shift reagent (SR) was investigated. This necessitated characterization of the following: first, the pool of Na<ce:inf>in</ce:inf>represented by the intracellular TQF (TQF<ce:inf>in</ce:inf>) spectrum; second, the maximum extent to which altered transverse relaxation times affect TQF<ce:inf>in</ce:inf>spectral amplitudes; and finally, the situations for which the SR-free method can reliably be applied. The rates of increase in peak amplitudes of both intracellular TQF spectra, adjusted for changes in both fast (<ce:italic>T</ce:italic><ce:inf>2f</ce:inf>) and slow (<ce:italic>T</ce:italic><ce:inf>2s</ce:inf>) transverse relaxation times, and intracellular single-quantum (SQ<ce:inf>in</ce:inf>) spectra were identical during no-flow ischemia, indicating that TQF<ce:inf>in</ce:inf>and SQ<ce:inf>in</ce:inf>spectra represent the same Na<ce:inf>in</ce:inf>population. Addition of an Na/K ATPase inhibitor, ouabain (≥500 μ<ce:italic>M</ce:italic>), and no-flow ischemia induced similar rates of increase of Na<ce:inf>in</ce:inf>content. However, the Na<ce:inf>in</ce:inf>level for which the<ce:italic>T</ce:italic><ce:inf>2</ce:inf>values started to increase was lower for ischemic (<140% of preischemic values) than for ouabain-exposed (>165%) hearts, which is consistent with the known earlier onset of intracellular swelling in ischemic hearts. Exposure of hearts to hyperosmotic perfusate (200 m<ce:italic>M</ce:italic>sucrose) increased [Na<ce:inf>in</ce:inf>], due to a decreased cell volume and an unchanged Na<ce:inf>in</ce:inf>content, but caused a decrease in<ce:italic>T</ce:italic><ce:inf>2</ce:inf>values, a trend opposite to that observed with exposure of hearts to ouabain or ischemia.<ce:italic>T</ce:italic><ce:inf>2</ce:inf>values therefore consistently correlated only with cell volume, not with Na<ce:inf>in</ce:inf>content or concentration, indicating an important role for intracellular macromolecule concentration in modulating transverse relaxation behavior. The combined effect of ischemia-induced increases in<ce:italic>T</ce:italic><ce:inf>2</ce:inf>values and their inhomogeneous broadened forms was an ∼6% overestimation of Na<ce:inf>in</ce:inf>content from amplitudes of SR-aided TQF<ce:inf>in</ce:inf>spectra, indicating negligible effect of transverse relaxation-dependent alterations on TQF<ce:inf>in</ce:inf>spectral amplitudes. Thus, Na<ce:inf>in</ce:inf>content may be reliably determined from SR-free TQF spectra when the contribution from extracellular Na does not appreciably vary, such as during constant pressure perfusion. Following complete reduction in perfusion pressure, both SR-free TQF and DQF spectra respond to increases in Na<ce:inf>in</ce:inf>content. However, SR-free DQF NMR provides an estimate of Na<ce:inf>in</ce:inf>content much closer to that provided by the SR-aided method, due to the appreciable decrease of the extracellular DQF signal resulting from destructive interference between second- and third-rank tensors.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Evaluation of Multiple-Quantum-Filtered23Na NMR in Monitoring Intracellular Na Content in the Isolated Perfused Rat Heart in the Absence of a Chemical-Shift Reagent</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Evaluation of Multiple-Quantum-Filtered</title></titleInfo><name type="personal"><namePart type="given">Joseph S.</namePart><namePart type="family">Tauskela</namePart><affiliation>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</affiliation><description>Present address: National Research Council, Institute for Biological Sciences, Building M-54, Montreal Road Campus, Ottawa, Ontario, Canada K1A 0R6.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">José M.</namePart><namePart type="family">Dizon</namePart><affiliation>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John</namePart><namePart type="family">Whang</namePart><affiliation>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">José</namePart><namePart type="family">Katz</namePart><affiliation>Department of Medicine, Division of Cardiology, College of Physicians & Surgeons, Columbia University, New York, New York</affiliation><description>To whom correspondence should be addressed: Department of Medicine, Division of Cardiology, Columbia University, PH 10-Stem, 630 West 168th Street, New York, NY 10032.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1997</dateIssued><dateModified encoding="w3cdtf">1997-04-10</dateModified><copyrightDate encoding="w3cdtf">1997</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: The feasibility of employing triple-quantum-filtered (TQF) or double-quantum-filtered (DQF)23Na NMR spectra to monitor intracellular Na (Nain) content in isolated rat hearts perfused in the absence of a chemical-shift reagent (SR) was investigated. This necessitated characterization of the following: first, the pool of Nainrepresented by the intracellular TQF (TQFin) spectrum; second, the maximum extent to which altered transverse relaxation times affect TQFinspectral amplitudes; and finally, the situations for which the SR-free method can reliably be applied. The rates of increase in peak amplitudes of both intracellular TQF spectra, adjusted for changes in both fast (T2f) and slow (T2s) transverse relaxation times, and intracellular single-quantum (SQin) spectra were identical during no-flow ischemia, indicating that TQFinand SQinspectra represent the same Nainpopulation. Addition of an Na/K ATPase inhibitor, ouabain (≥500 μM), and no-flow ischemia induced similar rates of increase of Naincontent. However, the Nainlevel for which theT2values started to increase was lower for ischemic (<140% of preischemic values) than for ouabain-exposed (>165%) hearts, which is consistent with the known earlier onset of intracellular swelling in ischemic hearts. Exposure of hearts to hyperosmotic perfusate (200 mMsucrose) increased [Nain], due to a decreased cell volume and an unchanged Naincontent, but caused a decrease inT2values, a trend opposite to that observed with exposure of hearts to ouabain or ischemia.T2values therefore consistently correlated only with cell volume, not with Naincontent or concentration, indicating an important role for intracellular macromolecule concentration in modulating transverse relaxation behavior. The combined effect of ischemia-induced increases inT2values and their inhomogeneous broadened forms was an ∼6% overestimation of Naincontent from amplitudes of SR-aided TQFinspectra, indicating negligible effect of transverse relaxation-dependent alterations on TQFinspectral amplitudes. Thus, Naincontent may be reliably determined from SR-free TQF spectra when the contribution from extracellular Na does not appreciably vary, such as during constant pressure perfusion. Following complete reduction in perfusion pressure, both SR-free TQF and DQF spectra respond to increases in Naincontent. However, SR-free DQF NMR provides an estimate of Naincontent much closer to that provided by the SR-aided method, due to the appreciable decrease of the extracellular DQF signal resulting from destructive interference between second- and third-rank tensors.</abstract><note type="content">Section title: Regular Article</note><relatedItem type="host"><titleInfo><title>Journal of Magnetic Resonance</title></titleInfo><titleInfo type="abbreviated"><title>YJMRE</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">199707</dateIssued></originInfo><identifier type="ISSN">1090-7807</identifier><identifier type="PII">S1090-7807(00)X0060-2</identifier><part><date>199707</date><detail type="volume"><number>127</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>137</end></extent><extent unit="pages"><start>115</start><end>127</end></extent></part></relatedItem><identifier type="istex">3C05A9E93E0F1B48AB7295845D12804B6E2E007D</identifier><identifier type="ark">ark:/67375/6H6-LKJSZC29-2</identifier><identifier type="DOI">10.1006/jmre.1997.1181</identifier><identifier type="PII">S1090-7807(97)91181-2</identifier><accessCondition type="use and reproduction" contentType="copyright">©1997 Academic Press</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Academic Press, ©1997</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/3C05A9E93E0F1B48AB7295845D12804B6E2E007D/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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