Fasting limits the increase in intracellular calcium during ischemia in isolated rat hearts.
Identifieur interne : 000721 ( PubMed/Corpus ); précédent : 000720; suivant : 000722Fasting limits the increase in intracellular calcium during ischemia in isolated rat hearts.
Auteurs : R. Ramasamy ; H. Liu ; G. Cherednichenko ; S. SchaeferSource :
- Basic research in cardiology [ 0300-8428 ] ; 2001.
English descriptors
- KwdEn :
- Animals, Blood Pressure, Calcium (metabolism), Calcium-Transporting ATPases (metabolism), Chelating Agents (pharmacology), Egtazic Acid (analogs & derivatives), Egtazic Acid (pharmacology), Fasting (physiology), In Vitro Techniques, Magnetic Resonance Spectroscopy, Myocardial Ischemia (metabolism), Myocardial Reperfusion Injury (metabolism), Myocardium (metabolism), Rats, Sarcoplasmic Reticulum (metabolism), Sodium (metabolism), Sodium-Calcium Exchanger (metabolism), Sodium-Potassium-Exchanging ATPase (metabolism).
- MESH :
- chemical , analogs & derivatives : Egtazic Acid.
- chemical , metabolism : Calcium, Calcium-Transporting ATPases, Sodium, Sodium-Calcium Exchanger, Sodium-Potassium-Exchanging ATPase.
- chemical , pharmacology : Chelating Agents, Egtazic Acid.
- metabolism : Myocardial Ischemia, Myocardial Reperfusion Injury, Myocardium, Sarcoplasmic Reticulum.
- physiology : Fasting.
- Animals, Blood Pressure, In Vitro Techniques, Magnetic Resonance Spectroscopy, Rats.
Abstract
Fasting has been shown to limit ischemic injury and improve functional activity after global ischemia. Because calcium overload is considered a mechanism of ischemic injury, we hypothesized that fasting would limit the accumulation of intracellular calcium [Ca]i during ischemia, potentially due to reduced accumulation of intracellular sodium [Na]i.
PubMed: 11605993
Links to Exploration step
pubmed:11605993Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Fasting limits the increase in intracellular calcium during ischemia in isolated rat hearts.</title><author><name sortKey="Ramasamy, R" sort="Ramasamy, R" uniqKey="Ramasamy R" first="R" last="Ramasamy">R. Ramasamy</name><affiliation><nlm:affiliation>Columbia University, Dept. of Cardiology, New York, NY 10032, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, H" sort="Liu, H" uniqKey="Liu H" first="H" last="Liu">H. Liu</name></author><author><name sortKey="Cherednichenko, G" sort="Cherednichenko, G" uniqKey="Cherednichenko G" first="G" last="Cherednichenko">G. Cherednichenko</name></author><author><name sortKey="Schaefer, S" sort="Schaefer, S" uniqKey="Schaefer S" first="S" last="Schaefer">S. Schaefer</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2001">2001</date><idno type="RBID">pubmed:11605993</idno><idno type="pmid">11605993</idno><idno type="wicri:Area/PubMed/Corpus">000721</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000721</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Fasting limits the increase in intracellular calcium during ischemia in isolated rat hearts.</title><author><name sortKey="Ramasamy, R" sort="Ramasamy, R" uniqKey="Ramasamy R" first="R" last="Ramasamy">R. Ramasamy</name><affiliation><nlm:affiliation>Columbia University, Dept. of Cardiology, New York, NY 10032, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, H" sort="Liu, H" uniqKey="Liu H" first="H" last="Liu">H. Liu</name></author><author><name sortKey="Cherednichenko, G" sort="Cherednichenko, G" uniqKey="Cherednichenko G" first="G" last="Cherednichenko">G. Cherednichenko</name></author><author><name sortKey="Schaefer, S" sort="Schaefer, S" uniqKey="Schaefer S" first="S" last="Schaefer">S. Schaefer</name></author></analytic><series><title level="j">Basic research in cardiology</title><idno type="ISSN">0300-8428</idno><imprint><date when="2001" type="published">2001</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Blood Pressure</term><term>Calcium (metabolism)</term><term>Calcium-Transporting ATPases (metabolism)</term><term>Chelating Agents (pharmacology)</term><term>Egtazic Acid (analogs & derivatives)</term><term>Egtazic Acid (pharmacology)</term><term>Fasting (physiology)</term><term>In Vitro Techniques</term><term>Magnetic Resonance Spectroscopy</term><term>Myocardial Ischemia (metabolism)</term><term>Myocardial Reperfusion Injury (metabolism)</term><term>Myocardium (metabolism)</term><term>Rats</term><term>Sarcoplasmic Reticulum (metabolism)</term><term>Sodium (metabolism)</term><term>Sodium-Calcium Exchanger (metabolism)</term><term>Sodium-Potassium-Exchanging ATPase (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Egtazic Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcium</term><term>Calcium-Transporting ATPases</term><term>Sodium</term><term>Sodium-Calcium Exchanger</term><term>Sodium-Potassium-Exchanging ATPase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chelating Agents</term><term>Egtazic Acid</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Myocardial Ischemia</term><term>Myocardial Reperfusion Injury</term><term>Myocardium</term><term>Sarcoplasmic Reticulum</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Fasting</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Blood Pressure</term><term>In Vitro Techniques</term><term>Magnetic Resonance Spectroscopy</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Fasting has been shown to limit ischemic injury and improve functional activity after global ischemia. Because calcium overload is considered a mechanism of ischemic injury, we hypothesized that fasting would limit the accumulation of intracellular calcium [Ca]i during ischemia, potentially due to reduced accumulation of intracellular sodium [Na]i.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">11605993</PMID><DateCreated><Year>2001</Year><Month>10</Month><Day>18</Day></DateCreated><DateCompleted><Year>2002</Year><Month>03</Month><Day>12</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0300-8428</ISSN><JournalIssue CitedMedium="Print"><Volume>96</Volume><Issue>5</Issue><PubDate><Year>2001</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Basic research in cardiology</Title><ISOAbbreviation>Basic Res. Cardiol.</ISOAbbreviation></Journal><ArticleTitle>Fasting limits the increase in intracellular calcium during ischemia in isolated rat hearts.</ArticleTitle><Pagination><MedlinePgn>463-70</MedlinePgn></Pagination><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Fasting has been shown to limit ischemic injury and improve functional activity after global ischemia. Because calcium overload is considered a mechanism of ischemic injury, we hypothesized that fasting would limit the accumulation of intracellular calcium [Ca]i during ischemia, potentially due to reduced accumulation of intracellular sodium [Na]i.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">To address this hypothesis, hearts isolated from rats fed either a normal diet or fasted for 24 hours underwent 20 min of global ischemia at 37 degrees. In addition to functional parameters, [Na]i and [Ca]i were measured using 21Na and 19F spectroscopy using thulium-DOTP-5 and 5F-BAPTA, respectively. In vitro measurement of sarcoplasmic reticulum calcium uptake and release, as well as activity of the sarcolemmal Na-Ca exchanger, was performed in hearts from fed and fasted animals under baseline and ischemic conditions.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Hearts from fasted animals showed greater recovery of developed pressure (37+/-9 vs. 11+/-6 cm H2O, p < 0.05) and less contracture (end-diastolic pressure 25+/-2 vs. 47+/-2 cm H2O, p < 0.05) by the end of the reperfusion period. [Na]i was similar in the 2 groups during the first half of the ischemic period, albeit with a higher concentration of [Na]i in hearts from fed compared to fasted animals at reperfusion. Fasting markedly limited calcium accumulation during ischemia, with end-ischemic calcium being 419+/-46 nM in the hearts from fasted animals and 858+/-140 nM in the hearts from fed animals (p < 0.01). There was no significant effect of fasting on calcium uptake or release by the SR, nor on sarcolemmal Na-Ca exchange activity.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Fasting for 24 hours improves functional recovery and markedly limits [Ca]i accumulation during ischemia and early reperfusion. The mechanism for this phenomenon remains to be elucidated.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ramasamy</LastName><ForeName>R</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Columbia University, Dept. of Cardiology, New York, NY 10032, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Cherednichenko</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Schaefer</LastName><ForeName>S</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HL 61783</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="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Basic Res Cardiol</MedlineTA><NlmUniqueID>0360342</NlmUniqueID><ISSNLinking>0300-8428</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002614">Chelating Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019831">Sodium-Calcium Exchanger</NameOfSubstance></Chemical><Chemical><RegistryNumber>526U7A2651</RegistryNumber><NameOfSubstance UI="D004533">Egtazic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>85233-21-2</RegistryNumber><NameOfSubstance UI="C039877">5,5'-difluoro-1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>9NEZ333N27</RegistryNumber><NameOfSubstance UI="D012964">Sodium</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.3.8</RegistryNumber><NameOfSubstance UI="D000252">Calcium-Transporting ATPases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.3.9</RegistryNumber><NameOfSubstance UI="D000254">Sodium-Potassium-Exchanging ATPase</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001794">Blood Pressure</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002118">Calcium</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000252">Calcium-Transporting ATPases</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002614">Chelating Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000494">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004533">Egtazic Acid</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000031">analogs & derivatives</QualifierName><QualifierName MajorTopicYN="N" UI="Q000494">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005215">Fasting</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D066298">In Vitro Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009682">Magnetic Resonance Spectroscopy</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017202">Myocardial Ischemia</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015428">Myocardial Reperfusion Injury</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009206">Myocardium</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012519">Sarcoplasmic Reticulum</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012964">Sodium</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019831">Sodium-Calcium Exchanger</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000254">Sodium-Potassium-Exchanging ATPase</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2001</Year><Month>10</Month><Day>19</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>3</Month><Day>13</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2001</Year><Month>10</Month><Day>19</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11605993</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Terre/explor/ThuliumV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000721 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 000721 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Terre
|area= ThuliumV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:11605993
|texte= Fasting limits the increase in intracellular calcium during ischemia in isolated rat hearts.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:11605993" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a ThuliumV1
| This area was generated with Dilib version V0.6.21. |  |