Effect of acute cardiac lymph stasis on metabolic coronary adaptation in the dog.
Identifieur interne : 006748 ( PubMed/Corpus ); précédent : 006747; suivant : 006749Effect of acute cardiac lymph stasis on metabolic coronary adaptation in the dog.
Auteurs : F. Solti ; V. Nemeth ; A. Juhasz-NagySource :
- Lymphology [ 0024-7766 ] ; 1985.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacology : Adenosine.
- drug effects : Coronary Circulation, Vasodilation.
- physiopathology : Lymphedema.
- Adaptation, Physiological, Animals, Dogs, Homeostasis.
Abstract
Surgical blockade of cardiac lymph drainage was performed in dogs to examine the effect of acute cardiac lymph stasis on coronary adaptive mechanisms. Coronary blood flow (CBF) was measured using an electromagnetic flow probe on the left anterior descending (LAD) artery. Metabolic autoregulatory capacity was assessed by eliciting reactive hyperemic responses after flow interruptions of 10-60 second duration and by administering submaximal doses (250-500 micrograms) of adenosine, the putative transmitter of reactive hyperemia, into the left heart. The effect of lymph stasis was tested in two experimental groups, one hour and 48 hours after lymph obstruction and the data compared to control dogs. Although cardiac lymph stasis did not notably affect baseline arterial pressure and CBF, both reactive hyperemic response and adenosine-induced coronary vasodilation were reduced significantly (equal to or less than 50% control). On occasion, a complete absence of autoregulation was observed. These findings suggest that cardiac lymph stasis decreases vascular responsiveness to physiologic vasodilator stimuli and/or retards diffusion of biologically unstable substance(s) presumably involved in autoregulation. Persistently impaired coronary autoregulation in the lymphedematous heart may contribute to progressive ischemic damage as for example after myocardial infarction.
PubMed: 4087936
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Juhasz-Nagy</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1985">1985</date><idno type="RBID">pubmed:4087936</idno><idno type="pmid">4087936</idno><idno type="wicri:Area/PubMed/Corpus">006748</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">006748</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effect of acute cardiac lymph stasis on metabolic coronary adaptation in the dog.</title><author><name sortKey="Solti, F" sort="Solti, F" uniqKey="Solti F" first="F" last="Solti">F. Solti</name></author><author><name sortKey="Nemeth, V" sort="Nemeth, V" uniqKey="Nemeth V" first="V" last="Nemeth">V. Nemeth</name></author><author><name sortKey="Juhasz Nagy, A" sort="Juhasz Nagy, A" uniqKey="Juhasz Nagy A" first="A" last="Juhasz-Nagy">A. Juhasz-Nagy</name></author></analytic><series><title level="j">Lymphology</title><idno type="ISSN">0024-7766</idno><imprint><date when="1985" type="published">1985</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptation, Physiological</term><term>Adenosine (pharmacology)</term><term>Animals</term><term>Coronary Circulation (drug effects)</term><term>Dogs</term><term>Homeostasis</term><term>Lymphedema (physiopathology)</term><term>Vasodilation (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenosine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Coronary Circulation</term><term>Vasodilation</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adaptation, Physiological</term><term>Animals</term><term>Dogs</term><term>Homeostasis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Surgical blockade of cardiac lymph drainage was performed in dogs to examine the effect of acute cardiac lymph stasis on coronary adaptive mechanisms. Coronary blood flow (CBF) was measured using an electromagnetic flow probe on the left anterior descending (LAD) artery. Metabolic autoregulatory capacity was assessed by eliciting reactive hyperemic responses after flow interruptions of 10-60 second duration and by administering submaximal doses (250-500 micrograms) of adenosine, the putative transmitter of reactive hyperemia, into the left heart. The effect of lymph stasis was tested in two experimental groups, one hour and 48 hours after lymph obstruction and the data compared to control dogs. Although cardiac lymph stasis did not notably affect baseline arterial pressure and CBF, both reactive hyperemic response and adenosine-induced coronary vasodilation were reduced significantly (equal to or less than 50% control). On occasion, a complete absence of autoregulation was observed. These findings suggest that cardiac lymph stasis decreases vascular responsiveness to physiologic vasodilator stimuli and/or retards diffusion of biologically unstable substance(s) presumably involved in autoregulation. Persistently impaired coronary autoregulation in the lymphedematous heart may contribute to progressive ischemic damage as for example after myocardial infarction.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">4087936</PMID><DateCreated><Year>1986</Year><Month>03</Month><Day>20</Day></DateCreated><DateCompleted><Year>1986</Year><Month>03</Month><Day>20</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0024-7766</ISSN><JournalIssue CitedMedium="Print"><Volume>18</Volume><Issue>3</Issue><PubDate><Year>1985</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Lymphology</Title><ISOAbbreviation>Lymphology</ISOAbbreviation></Journal><ArticleTitle>Effect of acute cardiac lymph stasis on metabolic coronary adaptation in the dog.</ArticleTitle><Pagination><MedlinePgn>136-42</MedlinePgn></Pagination><Abstract><AbstractText>Surgical blockade of cardiac lymph drainage was performed in dogs to examine the effect of acute cardiac lymph stasis on coronary adaptive mechanisms. Coronary blood flow (CBF) was measured using an electromagnetic flow probe on the left anterior descending (LAD) artery. Metabolic autoregulatory capacity was assessed by eliciting reactive hyperemic responses after flow interruptions of 10-60 second duration and by administering submaximal doses (250-500 micrograms) of adenosine, the putative transmitter of reactive hyperemia, into the left heart. The effect of lymph stasis was tested in two experimental groups, one hour and 48 hours after lymph obstruction and the data compared to control dogs. Although cardiac lymph stasis did not notably affect baseline arterial pressure and CBF, both reactive hyperemic response and adenosine-induced coronary vasodilation were reduced significantly (equal to or less than 50% control). On occasion, a complete absence of autoregulation was observed. These findings suggest that cardiac lymph stasis decreases vascular responsiveness to physiologic vasodilator stimuli and/or retards diffusion of biologically unstable substance(s) presumably involved in autoregulation. Persistently impaired coronary autoregulation in the lymphedematous heart may contribute to progressive ischemic damage as for example after myocardial infarction.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Solti</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Nemeth</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Juhasz-Nagy</LastName><ForeName>A</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Lymphology</MedlineTA><NlmUniqueID>0155112</NlmUniqueID><ISSNLinking>0024-7766</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>K72T3FS567</RegistryNumber><NameOfSubstance UI="D000241">Adenosine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000222" MajorTopicYN="N">Adaptation, Physiological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000241" MajorTopicYN="N">Adenosine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003326" MajorTopicYN="Y">Coronary Circulation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006706" MajorTopicYN="Y">Homeostasis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014664" MajorTopicYN="N">Vasodilation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1985</Year><Month>9</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1985</Year><Month>9</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1985</Year><Month>9</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">4087936</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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