Effect of lidocaine on contracture, intracellular sodium, and pH in ischemic rat hearts.
Identifieur interne : 000783 ( PubMed/Corpus ); précédent : 000782; suivant : 000784Effect of lidocaine on contracture, intracellular sodium, and pH in ischemic rat hearts.
Auteurs : N B Butwell ; R. Ramasamy ; I. Lazar ; A D Sherry ; C R MalloySource :
- The American journal of physiology [ 0002-9513 ] ; 1993.
English descriptors
- KwdEn :
- Animals, Cardiac Pacing, Artificial, Coronary Disease (metabolism), Coronary Disease (physiopathology), Hydrogen-Ion Concentration, Intracellular Membranes (metabolism), Lidocaine (pharmacology), Male, Myocardial Contraction (drug effects), Myocardium (metabolism), Phosphates (metabolism), Rats, Rats, Sprague-Dawley, Sodium (metabolism).
- MESH :
- chemical , metabolism : Phosphates, Sodium.
- chemical , pharmacology : Lidocaine.
- drug effects : Myocardial Contraction.
- metabolism : Coronary Disease, Intracellular Membranes, Myocardium.
- physiopathology : Coronary Disease.
- Animals, Cardiac Pacing, Artificial, Hydrogen-Ion Concentration, Male, Rats, Rats, Sprague-Dawley.
Abstract
The relationships among intracellular Na concentration ([Na+]i), intracellular pH, [ATP], and contracture during global ischemia were studied in isolated, perfused rat hearts. Intracellular Na was monitored by 23Na nuclear magnetic resonance (NMR) spectroscopy using thulium 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetra(methylene phosphonate) (TmDOTP5-) as the paramagnetic shift reagent. High-energy phosphates and pH were monitored under the same conditions using 31P-NMR spectroscopy. Lidocaine (130 microM), a class IB fast Na channel blocker known to protect ischemic myocardium, prolonged the time to contracture in both unpaced and paced hearts (240 beats/min). After 10 min of global ischemia in paced hearts, [Na+]i was lower in the lidocaine-treated group compared with untreated hearts. The addition of lidocaine also significantly attenuated the depletion of ATP as well as development of intracellular acidosis. At the time of contracture, however, there was no difference in [Na+]i or pH between the two groups. Interestingly, the effect of lidocaine on Na+i accumulation during ischemia was manifested during the first 5-10 min of ischemia, while its effect on pH occurred after 9 min. This finding suggests that a mechanism other than the Na-H exchanger may play a role in the accumulation of Na+i early in the course of ischemia.
PubMed: 8322918
Links to Exploration step
pubmed:8322918Le document en format XML
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Lazar</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="1993">1993</date><idno type="RBID">pubmed:8322918</idno><idno type="pmid">8322918</idno><idno type="wicri:Area/PubMed/Corpus">000783</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000783</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effect of lidocaine on contracture, intracellular sodium, and pH in ischemic rat hearts.</title><author><name sortKey="Butwell, N B" sort="Butwell, N B" uniqKey="Butwell N" first="N B" last="Butwell">N B Butwell</name><affiliation><nlm:affiliation>Department of Radiology, Mary Nell and Ralph B. Rogers Magnetic Resonance Center, University of Texas Southwestern Medical Center, Dallas.</nlm:affiliation></affiliation></author><author><name sortKey="Ramasamy, R" sort="Ramasamy, R" uniqKey="Ramasamy R" first="R" last="Ramasamy">R. Ramasamy</name></author><author><name sortKey="Lazar, I" sort="Lazar, I" uniqKey="Lazar I" first="I" last="Lazar">I. Lazar</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">The American journal of physiology</title><idno type="ISSN">0002-9513</idno><imprint><date when="1993" type="published">1993</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cardiac Pacing, Artificial</term><term>Coronary Disease (metabolism)</term><term>Coronary Disease (physiopathology)</term><term>Hydrogen-Ion Concentration</term><term>Intracellular Membranes (metabolism)</term><term>Lidocaine (pharmacology)</term><term>Male</term><term>Myocardial Contraction (drug effects)</term><term>Myocardium (metabolism)</term><term>Phosphates (metabolism)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Sodium (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Phosphates</term><term>Sodium</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Lidocaine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Myocardial Contraction</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Coronary Disease</term><term>Intracellular Membranes</term><term>Myocardium</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Coronary Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cardiac Pacing, Artificial</term><term>Hydrogen-Ion Concentration</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The relationships among intracellular Na concentration ([Na+]i), intracellular pH, [ATP], and contracture during global ischemia were studied in isolated, perfused rat hearts. Intracellular Na was monitored by 23Na nuclear magnetic resonance (NMR) spectroscopy using thulium 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetra(methylene phosphonate) (TmDOTP5-) as the paramagnetic shift reagent. High-energy phosphates and pH were monitored under the same conditions using 31P-NMR spectroscopy. Lidocaine (130 microM), a class IB fast Na channel blocker known to protect ischemic myocardium, prolonged the time to contracture in both unpaced and paced hearts (240 beats/min). After 10 min of global ischemia in paced hearts, [Na+]i was lower in the lidocaine-treated group compared with untreated hearts. The addition of lidocaine also significantly attenuated the depletion of ATP as well as development of intracellular acidosis. At the time of contracture, however, there was no difference in [Na+]i or pH between the two groups. Interestingly, the effect of lidocaine on Na+i accumulation during ischemia was manifested during the first 5-10 min of ischemia, while its effect on pH occurred after 9 min. This finding suggests that a mechanism other than the Na-H exchanger may play a role in the accumulation of Na+i early in the course of ischemia.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">8322918</PMID><DateCreated><Year>1993</Year><Month>08</Month><Day>05</Day></DateCreated><DateCompleted><Year>1993</Year><Month>08</Month><Day>05</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0002-9513</ISSN><JournalIssue CitedMedium="Print"><Volume>264</Volume><Issue>6 Pt 2</Issue><PubDate><Year>1993</Year><Month>Jun</Month></PubDate></JournalIssue><Title>The American journal of physiology</Title><ISOAbbreviation>Am. J. Physiol.</ISOAbbreviation></Journal><ArticleTitle>Effect of lidocaine on contracture, intracellular sodium, and pH in ischemic rat hearts.</ArticleTitle><Pagination><MedlinePgn>H1884-9</MedlinePgn></Pagination><Abstract><AbstractText>The relationships among intracellular Na concentration ([Na+]i), intracellular pH, [ATP], and contracture during global ischemia were studied in isolated, perfused rat hearts. Intracellular Na was monitored by 23Na nuclear magnetic resonance (NMR) spectroscopy using thulium 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetra(methylene phosphonate) (TmDOTP5-) as the paramagnetic shift reagent. High-energy phosphates and pH were monitored under the same conditions using 31P-NMR spectroscopy. Lidocaine (130 microM), a class IB fast Na channel blocker known to protect ischemic myocardium, prolonged the time to contracture in both unpaced and paced hearts (240 beats/min). After 10 min of global ischemia in paced hearts, [Na+]i was lower in the lidocaine-treated group compared with untreated hearts. The addition of lidocaine also significantly attenuated the depletion of ATP as well as development of intracellular acidosis. At the time of contracture, however, there was no difference in [Na+]i or pH between the two groups. Interestingly, the effect of lidocaine on Na+i accumulation during ischemia was manifested during the first 5-10 min of ischemia, while its effect on pH occurred after 9 min. This finding suggests that a mechanism other than the Na-H exchanger may play a role in the accumulation of Na+i early in the course of ischemia.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Butwell</LastName><ForeName>N B</ForeName><Initials>NB</Initials><AffiliationInfo><Affiliation>Department of Radiology, Mary Nell and Ralph B. 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