Effects of ischemia on intracellular sodium and phosphates in the in vivo rat liver.
Identifieur interne : 000740 ( PubMed/Checkpoint ); précédent : 000739; suivant : 000741Effects of ischemia on intracellular sodium and phosphates in the in vivo rat liver.
Auteurs : Z F Xia [États-Unis] ; J W Horton ; P Y Zhao ; E E Babcock ; A D Sherry ; C R MalloySource :
- Journal of applied physiology (Bethesda, Md. : 1985) [ 8750-7587 ] ; 1996.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Adenosine Triphosphate, Phosphates, Sodium.
- metabolism : Ischemia, Liver.
- Animals, Hydrogen-Ion Concentration, Magnetic Resonance Spectroscopy, Male, Rats, Rats, Sprague-Dawley.
Abstract
Metabolic factors that influence the transition form reversible to irreversible ischemic injury were studied in the rat liver in vivo with 31P-nuclear magnetic resonance (NMR) spectroscopy. Hepatic ischemia for 15, 35, or 65 min was produced by occlusion of the hepatic artery and portal vein in rats. Ischemia caused a rapid decrease in the ATP concentration ([ATP])-to-P(i) concentration ratio and pH within 5 min, but there was little change in these variables detectable by 31P-NMR with longer periods of ischemia. After reperfusion, the [ATP] and P(i) concentration returned toward normal values in livers exposed to 15 or 35 min of ischemia, but 65 min of ischemia were associated with only modest recovery in [ATP], and the [ATP] later decreased. Because the 31P-NMR spectrum was similar after brief compared with prolonged ischemia, it appears that neither ATP depletion, P(i) accumulation, nor acidosis predicts metabolic recovery. Hepatic intracellular NA+ was also measured in separate groups of animals by 23Na-NMR in the presence of a shift agent, thulium (III) 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetrakis (methylene-phosphonate) (TmDOTP5-), and by atomic absorption spectroscopy. Under baseline conditions, the concentration of intracellular Na+ was 15.2 mM by atomic absorption spectroscopy and 16.5 mM by 23Na-NMR. Although the 31P-NMR spectrum responded very rapidly to the onset of ischemia, intracellular Na+ concentration measured by 23Na-NMR increased gradually but steadily at approximately 1.0 mM/min during early (up to 15 min) ischemia. These observations demonstrate that a rise in intracellular Na+ does occur early ischemia, that TmDOTP5- can be applied in vivo for analysis of intracellular Na+ in the ischemic liver, and that 31P-NMR spectroscopy is very sensitive to early ischemic injury.
PubMed: 8889779
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Rogers Magnetic Resonance Center, Dallas, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Horton, J W" sort="Horton, J W" uniqKey="Horton J" first="J W" last="Horton">J W Horton</name></author><author><name sortKey="Zhao, P Y" sort="Zhao, P Y" uniqKey="Zhao P" first="P Y" last="Zhao">P Y Zhao</name></author><author><name sortKey="Babcock, E E" sort="Babcock, E E" uniqKey="Babcock E" first="E E" last="Babcock">E E Babcock</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><author><name sortKey="Malloy, C R" sort="Malloy, C R" uniqKey="Malloy C" first="C R" last="Malloy">C R Malloy</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1996">1996</date><idno type="RBID">pubmed:8889779</idno><idno type="pmid">8889779</idno><idno type="wicri:Area/PubMed/Corpus">000758</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000758</idno><idno type="wicri:Area/PubMed/Curation">000758</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000758</idno><idno type="wicri:Area/PubMed/Checkpoint">000758</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000758</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effects of ischemia on intracellular sodium and phosphates in the in vivo rat liver.</title><author><name sortKey="Xia, Z F" sort="Xia, Z F" uniqKey="Xia Z" first="Z F" last="Xia">Z F Xia</name><affiliation wicri:level="2"><nlm:affiliation>Department of Surgery, Mary Nell and Ralph B. Rogers Magnetic Resonance Center, Dallas, Texas, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Surgery, Mary Nell and Ralph B. Rogers Magnetic Resonance Center, Dallas, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Horton, J W" sort="Horton, J W" uniqKey="Horton J" first="J W" last="Horton">J W Horton</name></author><author><name sortKey="Zhao, P Y" sort="Zhao, P Y" uniqKey="Zhao P" first="P Y" last="Zhao">P Y Zhao</name></author><author><name sortKey="Babcock, E E" sort="Babcock, E E" uniqKey="Babcock E" first="E E" last="Babcock">E E Babcock</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><author><name sortKey="Malloy, C R" sort="Malloy, C R" uniqKey="Malloy C" first="C R" last="Malloy">C R Malloy</name></author></analytic><series><title level="j">Journal of applied physiology (Bethesda, Md. : 1985)</title><idno type="ISSN">8750-7587</idno><imprint><date when="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosine Triphosphate (metabolism)</term><term>Animals</term><term>Hydrogen-Ion Concentration</term><term>Ischemia (metabolism)</term><term>Liver (metabolism)</term><term>Magnetic Resonance Spectroscopy</term><term>Male</term><term>Phosphates (metabolism)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Sodium (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adénosine triphosphate (métabolisme)</term><term>Animaux</term><term>Concentration en ions d'hydrogène</term><term>Foie (métabolisme)</term><term>Ischémie (métabolisme)</term><term>Mâle</term><term>Phosphates (métabolisme)</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Sodium (métabolisme)</term><term>Spectroscopie par résonance magnétique</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenosine Triphosphate</term><term>Phosphates</term><term>Sodium</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Ischemia</term><term>Liver</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Adénosine triphosphate</term><term>Foie</term><term>Ischémie</term><term>Phosphates</term><term>Sodium</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Hydrogen-Ion Concentration</term><term>Magnetic Resonance Spectroscopy</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Concentration en ions d'hydrogène</term><term>Mâle</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Spectroscopie par résonance magnétique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Metabolic factors that influence the transition form reversible to irreversible ischemic injury were studied in the rat liver in vivo with 31P-nuclear magnetic resonance (NMR) spectroscopy. Hepatic ischemia for 15, 35, or 65 min was produced by occlusion of the hepatic artery and portal vein in rats. Ischemia caused a rapid decrease in the ATP concentration ([ATP])-to-P(i) concentration ratio and pH within 5 min, but there was little change in these variables detectable by 31P-NMR with longer periods of ischemia. After reperfusion, the [ATP] and P(i) concentration returned toward normal values in livers exposed to 15 or 35 min of ischemia, but 65 min of ischemia were associated with only modest recovery in [ATP], and the [ATP] later decreased. Because the 31P-NMR spectrum was similar after brief compared with prolonged ischemia, it appears that neither ATP depletion, P(i) accumulation, nor acidosis predicts metabolic recovery. Hepatic intracellular NA+ was also measured in separate groups of animals by 23Na-NMR in the presence of a shift agent, thulium (III) 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetrakis (methylene-phosphonate) (TmDOTP5-), and by atomic absorption spectroscopy. Under baseline conditions, the concentration of intracellular Na+ was 15.2 mM by atomic absorption spectroscopy and 16.5 mM by 23Na-NMR. Although the 31P-NMR spectrum responded very rapidly to the onset of ischemia, intracellular Na+ concentration measured by 23Na-NMR increased gradually but steadily at approximately 1.0 mM/min during early (up to 15 min) ischemia. These observations demonstrate that a rise in intracellular Na+ does occur early ischemia, that TmDOTP5- can be applied in vivo for analysis of intracellular Na+ in the ischemic liver, and that 31P-NMR spectroscopy is very sensitive to early ischemic injury.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">8889779</PMID><DateCreated><Year>1997</Year><Month>02</Month><Day>07</Day></DateCreated><DateCompleted><Year>1997</Year><Month>02</Month><Day>07</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">8750-7587</ISSN><JournalIssue CitedMedium="Print"><Volume>81</Volume><Issue>3</Issue><PubDate><Year>1996</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Journal of applied physiology (Bethesda, Md. : 1985)</Title><ISOAbbreviation>J. Appl. Physiol.</ISOAbbreviation></Journal><ArticleTitle>Effects of ischemia on intracellular sodium and phosphates in the in vivo rat liver.</ArticleTitle><Pagination><MedlinePgn>1395-403</MedlinePgn></Pagination><Abstract><AbstractText>Metabolic factors that influence the transition form reversible to irreversible ischemic injury were studied in the rat liver in vivo with 31P-nuclear magnetic resonance (NMR) spectroscopy. Hepatic ischemia for 15, 35, or 65 min was produced by occlusion of the hepatic artery and portal vein in rats. Ischemia caused a rapid decrease in the ATP concentration ([ATP])-to-P(i) concentration ratio and pH within 5 min, but there was little change in these variables detectable by 31P-NMR with longer periods of ischemia. After reperfusion, the [ATP] and P(i) concentration returned toward normal values in livers exposed to 15 or 35 min of ischemia, but 65 min of ischemia were associated with only modest recovery in [ATP], and the [ATP] later decreased. Because the 31P-NMR spectrum was similar after brief compared with prolonged ischemia, it appears that neither ATP depletion, P(i) accumulation, nor acidosis predicts metabolic recovery. Hepatic intracellular NA+ was also measured in separate groups of animals by 23Na-NMR in the presence of a shift agent, thulium (III) 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetrakis (methylene-phosphonate) (TmDOTP5-), and by atomic absorption spectroscopy. Under baseline conditions, the concentration of intracellular Na+ was 15.2 mM by atomic absorption spectroscopy and 16.5 mM by 23Na-NMR. Although the 31P-NMR spectrum responded very rapidly to the onset of ischemia, intracellular Na+ concentration measured by 23Na-NMR increased gradually but steadily at approximately 1.0 mM/min during early (up to 15 min) ischemia. These observations demonstrate that a rise in intracellular Na+ does occur early ischemia, that TmDOTP5- can be applied in vivo for analysis of intracellular Na+ in the ischemic liver, and that 31P-NMR spectroscopy is very sensitive to early ischemic injury.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Xia</LastName><ForeName>Z F</ForeName><Initials>ZF</Initials><AffiliationInfo><Affiliation>Department of Surgery, Mary Nell and Ralph B. Rogers Magnetic Resonance Center, Dallas, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Horton</LastName><ForeName>J W</ForeName><Initials>JW</Initials></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>P Y</ForeName><Initials>PY</Initials></Author><Author ValidYN="Y"><LastName>Babcock</LastName><ForeName>E E</ForeName><Initials>EE</Initials></Author><Author ValidYN="Y"><LastName>Sherry</LastName><ForeName>A D</ForeName><Initials>AD</Initials></Author><Author ValidYN="Y"><LastName>Malloy</LastName><ForeName>C R</ForeName><Initials>CR</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HL-34557</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41-RR-02584</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</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>J Appl Physiol (1985)</MedlineTA><NlmUniqueID>8502536</NlmUniqueID><ISSNLinking>0161-7567</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010710">Phosphates</NameOfSubstance></Chemical><Chemical><RegistryNumber>8L70Q75FXE</RegistryNumber><NameOfSubstance UI="D000255">Adenosine Triphosphate</NameOfSubstance></Chemical><Chemical><RegistryNumber>9NEZ333N27</RegistryNumber><NameOfSubstance UI="D012964">Sodium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000255">Adenosine Triphosphate</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006863">Hydrogen-Ion Concentration</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007511">Ischemia</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008099">Liver</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></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="D010710">Phosphates</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017207">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012964">Sodium</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1996</Year><Month>9</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1996</Year><Month>9</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1996</Year><Month>9</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8889779</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Texas</li></region></list><tree><noCountry><name sortKey="Babcock, E E" sort="Babcock, E E" uniqKey="Babcock E" first="E E" last="Babcock">E E Babcock</name><name sortKey="Horton, J W" sort="Horton, J W" uniqKey="Horton J" first="J W" last="Horton">J W Horton</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><name sortKey="Zhao, P Y" sort="Zhao, P Y" uniqKey="Zhao P" first="P Y" last="Zhao">P Y Zhao</name></noCountry><country name="États-Unis"><region name="Texas"><name sortKey="Xia, Z F" sort="Xia, Z F" uniqKey="Xia Z" first="Z F" last="Xia">Z F Xia</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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