Influence of global ischemia on intracellular sodium in the perfused rat heart.
Identifieur interne : 000794 ( PubMed/Checkpoint ); précédent : 000793; suivant : 000795Influence of global ischemia on intracellular sodium in the perfused rat heart.
Auteurs : C R Malloy ; D C Buster ; M M Castro ; C F Geraldes ; F M Jeffrey ; A D SherrySource :
- Magnetic resonance in medicine [ 0740-3194 ] ; 1990.
Descripteurs français
- KwdFr :
- MESH :
- analyse : Myocarde, Sodium.
- métabolisme : Maladie coronarienne.
- Animaux, Coeur, Lignées consanguines de rats, Mâle, Oxazoles, Perfusion, Pyrimidinones, Rats, Spectrophotométrie atomique, Spectroscopie par résonance magnétique, Thulium.
English descriptors
- KwdEn :
- MESH :
- chemical , analysis : Sodium.
- chemical : Oxazoles, Pyrimidinones, Thulium.
- analysis : Myocardium.
- metabolism : Coronary Disease.
- Animals, Heart, Magnetic Resonance Spectroscopy, Male, Perfusion, Rats, Rats, Inbred Strains, Spectrophotometry, Atomic.
Abstract
Intracellular [Na+], [H+], and [ATP] and mechanical performance were measured in the isovolumic perfused rat heart during ischemia. The concentration of intracellular sodium, [Na+]i, was determined by atomic absorption spectroscopy under control conditions, and [Na+]i was monitored by 23Na NMR spectroscopy at 1-min intervals under control conditions and during global ischemia. [ATP], [H+], and [Pi] were measured by 31P NMR in a separate group under identical conditions. The control [Na+]i measured by atomic absorption was 30.7 +/- 3.3 mM (mean +/- SD, n = 6), and [Na+]i measured by NMR was 6.2 +/- 0.5 mM (n = 3). Brief ischemia (10 min) was associated with a 54% increase in [Na+]i which reversed completely with reperfusion. Developed pressure also returned to control values upon reperfusion. Prolonged ischemia (30 min) produced continuous further accumulation of sodium (0.53 mM/min, r2 = 0.99). [H+] also increased approximately linearly early in ischemia (0.084 microM/min, r2 = 0.97). The rate of increase in [Na+]i was more than 4000 times greater than the increase in [H+] on a molar basis. Nevertheless, [H+]/[Na+]i increased early in ischemia because the proportional change in [H+] was greater than that in [Na+]i. These results indicate that (1) intracellular sodium measured by NMR in the functioning heart is about 20% of total intracellular sodium; (2) intracellular acidosis and accumulation of sodium develop simultaneously during global ischemia; (3) increased intracellular sodium content is not in itself an indicator of irreversible injury; and (4) recovery of mechanical performance is associated with return of [Na+]i (measured by NMR) to baseline after brief ischemia. The mechanism of the increase in sodium content detected by NMR is unknown.
PubMed: 2374498
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first="F M" last="Jeffrey">F M Jeffrey</name></author><author><name sortKey="Sherry, A D" sort="Sherry, A D" uniqKey="Sherry A" first="A D" last="Sherry">A D Sherry</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1990">1990</date><idno type="RBID">pubmed:2374498</idno><idno type="pmid">2374498</idno><idno type="wicri:Area/PubMed/Corpus">000819</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000819</idno><idno type="wicri:Area/PubMed/Curation">000819</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000819</idno><idno type="wicri:Area/PubMed/Checkpoint">000819</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000819</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Influence of global ischemia on intracellular sodium in the perfused rat heart.</title><author><name sortKey="Malloy, C R" sort="Malloy, C R" uniqKey="Malloy C" first="C R" last="Malloy">C R Malloy</name><affiliation><nlm:affiliation>Department of Internal Medicine (Cardiology Division), University of Texas Southwestern Medical Center, Dallas 75235-9047.</nlm:affiliation><wicri:noCountry code="subField">Dallas 75235-9047</wicri:noCountry></affiliation></author><author><name sortKey="Buster, D C" sort="Buster, D C" uniqKey="Buster D" first="D C" last="Buster">D C Buster</name></author><author><name sortKey="Castro, M M" sort="Castro, M M" uniqKey="Castro M" first="M M" last="Castro">M M Castro</name></author><author><name sortKey="Geraldes, C F" sort="Geraldes, C F" uniqKey="Geraldes C" first="C F" last="Geraldes">C F Geraldes</name></author><author><name sortKey="Jeffrey, F M" sort="Jeffrey, F M" uniqKey="Jeffrey F" first="F M" last="Jeffrey">F M Jeffrey</name></author><author><name sortKey="Sherry, A D" sort="Sherry, A D" uniqKey="Sherry A" first="A D" last="Sherry">A D Sherry</name></author></analytic><series><title level="j">Magnetic resonance in medicine</title><idno type="ISSN">0740-3194</idno><imprint><date when="1990" type="published">1990</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Coronary Disease (metabolism)</term><term>Heart</term><term>Magnetic Resonance Spectroscopy</term><term>Male</term><term>Myocardium (analysis)</term><term>Oxazoles</term><term>Perfusion</term><term>Pyrimidinones</term><term>Rats</term><term>Rats, Inbred Strains</term><term>Sodium (analysis)</term><term>Spectrophotometry, Atomic</term><term>Thulium</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Coeur</term><term>Lignées consanguines de rats</term><term>Maladie coronarienne (métabolisme)</term><term>Myocarde (analyse)</term><term>Mâle</term><term>Oxazoles</term><term>Perfusion</term><term>Pyrimidinones</term><term>Rats</term><term>Sodium (analyse)</term><term>Spectrophotométrie atomique</term><term>Spectroscopie par résonance magnétique</term><term>Thulium</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Sodium</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Oxazoles</term><term>Pyrimidinones</term><term>Thulium</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Myocarde</term><term>Sodium</term></keywords><keywords scheme="MESH" qualifier="analysis" xml:lang="en"><term>Myocardium</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Coronary Disease</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Maladie coronarienne</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Heart</term><term>Magnetic Resonance Spectroscopy</term><term>Male</term><term>Perfusion</term><term>Rats</term><term>Rats, Inbred Strains</term><term>Spectrophotometry, Atomic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Coeur</term><term>Lignées consanguines de rats</term><term>Mâle</term><term>Oxazoles</term><term>Perfusion</term><term>Pyrimidinones</term><term>Rats</term><term>Spectrophotométrie atomique</term><term>Spectroscopie par résonance magnétique</term><term>Thulium</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Intracellular [Na+], [H+], and [ATP] and mechanical performance were measured in the isovolumic perfused rat heart during ischemia. The concentration of intracellular sodium, [Na+]i, was determined by atomic absorption spectroscopy under control conditions, and [Na+]i was monitored by 23Na NMR spectroscopy at 1-min intervals under control conditions and during global ischemia. [ATP], [H+], and [Pi] were measured by 31P NMR in a separate group under identical conditions. The control [Na+]i measured by atomic absorption was 30.7 +/- 3.3 mM (mean +/- SD, n = 6), and [Na+]i measured by NMR was 6.2 +/- 0.5 mM (n = 3). Brief ischemia (10 min) was associated with a 54% increase in [Na+]i which reversed completely with reperfusion. Developed pressure also returned to control values upon reperfusion. Prolonged ischemia (30 min) produced continuous further accumulation of sodium (0.53 mM/min, r2 = 0.99). [H+] also increased approximately linearly early in ischemia (0.084 microM/min, r2 = 0.97). The rate of increase in [Na+]i was more than 4000 times greater than the increase in [H+] on a molar basis. Nevertheless, [H+]/[Na+]i increased early in ischemia because the proportional change in [H+] was greater than that in [Na+]i. These results indicate that (1) intracellular sodium measured by NMR in the functioning heart is about 20% of total intracellular sodium; (2) intracellular acidosis and accumulation of sodium develop simultaneously during global ischemia; (3) increased intracellular sodium content is not in itself an indicator of irreversible injury; and (4) recovery of mechanical performance is associated with return of [Na+]i (measured by NMR) to baseline after brief ischemia. The mechanism of the increase in sodium content detected by NMR is unknown.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">2374498</PMID><DateCreated><Year>1990</Year><Month>08</Month><Day>29</Day></DateCreated><DateCompleted><Year>1990</Year><Month>08</Month><Day>29</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0740-3194</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><Issue>1</Issue><PubDate><Year>1990</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Magnetic resonance in medicine</Title><ISOAbbreviation>Magn Reson Med</ISOAbbreviation></Journal><ArticleTitle>Influence of global ischemia on intracellular sodium in the perfused rat heart.</ArticleTitle><Pagination><MedlinePgn>33-44</MedlinePgn></Pagination><Abstract><AbstractText>Intracellular [Na+], [H+], and [ATP] and mechanical performance were measured in the isovolumic perfused rat heart during ischemia. The concentration of intracellular sodium, [Na+]i, was determined by atomic absorption spectroscopy under control conditions, and [Na+]i was monitored by 23Na NMR spectroscopy at 1-min intervals under control conditions and during global ischemia. [ATP], [H+], and [Pi] were measured by 31P NMR in a separate group under identical conditions. The control [Na+]i measured by atomic absorption was 30.7 +/- 3.3 mM (mean +/- SD, n = 6), and [Na+]i measured by NMR was 6.2 +/- 0.5 mM (n = 3). Brief ischemia (10 min) was associated with a 54% increase in [Na+]i which reversed completely with reperfusion. Developed pressure also returned to control values upon reperfusion. Prolonged ischemia (30 min) produced continuous further accumulation of sodium (0.53 mM/min, r2 = 0.99). [H+] also increased approximately linearly early in ischemia (0.084 microM/min, r2 = 0.97). The rate of increase in [Na+]i was more than 4000 times greater than the increase in [H+] on a molar basis. Nevertheless, [H+]/[Na+]i increased early in ischemia because the proportional change in [H+] was greater than that in [Na+]i. These results indicate that (1) intracellular sodium measured by NMR in the functioning heart is about 20% of total intracellular sodium; (2) intracellular acidosis and accumulation of sodium develop simultaneously during global ischemia; (3) increased intracellular sodium content is not in itself an indicator of irreversible injury; and (4) recovery of mechanical performance is associated with return of [Na+]i (measured by NMR) to baseline after brief ischemia. The mechanism of the increase in sodium content detected by NMR is unknown.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Malloy</LastName><ForeName>C R</ForeName><Initials>CR</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine (Cardiology Division), University of Texas Southwestern Medical Center, Dallas 75235-9047.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Buster</LastName><ForeName>D C</ForeName><Initials>DC</Initials></Author><Author ValidYN="Y"><LastName>Castro</LastName><ForeName>M M</ForeName><Initials>MM</Initials></Author><Author ValidYN="Y"><LastName>Geraldes</LastName><ForeName>C F</ForeName><Initials>CF</Initials></Author><Author ValidYN="Y"><LastName>Jeffrey</LastName><ForeName>F M</ForeName><Initials>FM</Initials></Author><Author ValidYN="Y"><LastName>Sherry</LastName><ForeName>A D</ForeName><Initials>AD</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01-HL34557</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Magn Reson Med</MedlineTA><NlmUniqueID>8505245</NlmUniqueID><ISSNLinking>0740-3194</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010080">Oxazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011744">Pyrimidinones</NameOfSubstance></Chemical><Chemical><RegistryNumber>123495-11-4</RegistryNumber><NameOfSubstance UI="C063359">2,3-dihydro-5H-oxazolo(3,2-a)thieno(3,2-d)pyrimidin-5-one</NameOfSubstance></Chemical><Chemical><RegistryNumber>8RKC5ATI4P</RegistryNumber><NameOfSubstance UI="D013932">Thulium</NameOfSubstance></Chemical><Chemical><RegistryNumber>9NEZ333N27</RegistryNumber><NameOfSubstance UI="D012964">Sodium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003327">Coronary Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006321">Heart</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009682">Magnetic Resonance Spectroscopy</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009206">Myocardium</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000032">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010080">Oxazoles</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010477">Perfusion</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011744">Pyrimidinones</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011919">Rats, Inbred Strains</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012964">Sodium</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000032">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013054">Spectrophotometry, Atomic</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013932">Thulium</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1990</Year><Month>7</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1990</Year><Month>7</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1990</Year><Month>7</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">2374498</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Buster, D C" sort="Buster, D C" uniqKey="Buster D" first="D C" last="Buster">D C Buster</name><name sortKey="Castro, M M" sort="Castro, M M" uniqKey="Castro M" first="M M" last="Castro">M M Castro</name><name sortKey="Geraldes, C F" sort="Geraldes, C F" uniqKey="Geraldes C" first="C F" last="Geraldes">C F Geraldes</name><name sortKey="Jeffrey, F M" sort="Jeffrey, F M" uniqKey="Jeffrey F" first="F M" last="Jeffrey">F M Jeffrey</name><name sortKey="Malloy, C R" sort="Malloy, C R" uniqKey="Malloy C" first="C R" last="Malloy">C R Malloy</name><name sortKey="Sherry, A D" sort="Sherry, A D" uniqKey="Sherry A" first="A D" last="Sherry">A D Sherry</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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