A chronic and latent lymphatic insufficiency follows recovery from acute lymphedema in the rat foreleg.
Identifieur interne : 001F77 ( PubMed/Corpus ); précédent : 001F76; suivant : 001F78A chronic and latent lymphatic insufficiency follows recovery from acute lymphedema in the rat foreleg.
Auteurs : Uziel Mendez ; Emily M. Stroup ; Laura L. Lynch ; Anna B. Waller ; Jeremy GoldmanSource :
- American journal of physiology. Heart and circulatory physiology [ 1522-1539 ] ; 2012.
English descriptors
- KwdEn :
- Acute Disease, Animals, Female, Forelimb, Inflammation (chemically induced), Inflammation (complications), Lymph Node Excision (adverse effects), Lymphatic System (drug effects), Lymphatic System (physiopathology), Lymphedema (etiology), Lymphedema (physiopathology), Lymphography, Models, Animal, Oxazolone (adverse effects), Oxazolone (pharmacology), Rats, Rats, Sprague-Dawley.
- MESH :
- chemical , adverse effects : Oxazolone.
- adverse effects : Lymph Node Excision.
- chemically induced : Inflammation.
- complications : Inflammation.
- drug effects : Lymphatic System.
- etiology : Lymphedema.
- chemical , pharmacology : Oxazolone.
- physiopathology : Lymphatic System, Lymphedema.
- Acute Disease, Animals, Female, Forelimb, Lymphography, Models, Animal, Rats, Rats, Sprague-Dawley.
Abstract
Secondary lymphedema in humans is a common consequence of axillary lymph node dissection (ALND) to treat breast cancer. Remarkably, secondary lymphedema generally first appears following a delay of over a year and can be triggered suddenly by an inflammatory insult. However, it remains unclear why the apparently functional lymphatic system is unable to accommodate an inflammatory trigger. To provide mechanistic insight into the delayed and rapid secondary lymphedema initiation, we compared the ability of the ALND-recovered rat foreleg lymphatic system to prevent edema during an inflammatory challenge with that of the uninjured lymphatic system. At 73 days postsurgery, the forelegs of ALND(-)- and ALND(+)-sensitized rats were exposed to the proinflammatory agent oxazolone, which was found to reduce fluid drainage and increase skin thickness in both ALND(-) and ALND(+) forelegs (P < 0.05). However, drainage in the ALND-recovered forelegs was more severely impaired than ALND(-) forelegs, as visualized by indocyanine green lymphography and quantified by interstitial transport of fluid marker (P < 0.05). Although both ALND(+) and ALND(-) forelegs experienced significant inflammation-induced edema with the oxazolone exposure (P < 0.05), the peak tissue swelling in the ALND(+) group was significantly greater than that of the ALND(-) forelegs (arm area peaked at ∼13.4 vs. ∼5.7% swelling, respectively, P < 0.005; wrist diameter peaked at 9.7 vs. 2.2% swelling, respectively, P < 0.005). The findings demonstrate that outward recovery from ALND in the rat foreleg masks an ensuing chronic and latent lymphatic insufficiency, which reduces the ability of the foreleg lymphatic system to prevent edema during an acute inflammatory process.
DOI: 10.1152/ajpheart.00522.2012
PubMed: 22942182
Links to Exploration step
pubmed:22942182Le document en format XML
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Waller</name></author><author><name sortKey="Goldman, Jeremy" sort="Goldman, Jeremy" uniqKey="Goldman J" first="Jeremy" last="Goldman">Jeremy Goldman</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:22942182</idno><idno type="pmid">22942182</idno><idno type="doi">10.1152/ajpheart.00522.2012</idno><idno type="wicri:Area/PubMed/Corpus">001F77</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001F77</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">A chronic and latent lymphatic insufficiency follows recovery from acute lymphedema in the rat foreleg.</title><author><name sortKey="Mendez, Uziel" sort="Mendez, Uziel" uniqKey="Mendez U" first="Uziel" last="Mendez">Uziel Mendez</name><affiliation><nlm:affiliation>Biomedical Engineering Department, Michigan Technological University, Houghton, Michigan 49931, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Stroup, Emily M" sort="Stroup, Emily M" uniqKey="Stroup E" first="Emily M" last="Stroup">Emily M. Stroup</name></author><author><name sortKey="Lynch, Laura L" sort="Lynch, Laura L" uniqKey="Lynch L" first="Laura L" last="Lynch">Laura L. Lynch</name></author><author><name sortKey="Waller, Anna B" sort="Waller, Anna B" uniqKey="Waller A" first="Anna B" last="Waller">Anna B. Waller</name></author><author><name sortKey="Goldman, Jeremy" sort="Goldman, Jeremy" uniqKey="Goldman J" first="Jeremy" last="Goldman">Jeremy Goldman</name></author></analytic><series><title level="j">American journal of physiology. Heart and circulatory physiology</title><idno type="eISSN">1522-1539</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Disease</term><term>Animals</term><term>Female</term><term>Forelimb</term><term>Inflammation (chemically induced)</term><term>Inflammation (complications)</term><term>Lymph Node Excision (adverse effects)</term><term>Lymphatic System (drug effects)</term><term>Lymphatic System (physiopathology)</term><term>Lymphedema (etiology)</term><term>Lymphedema (physiopathology)</term><term>Lymphography</term><term>Models, Animal</term><term>Oxazolone (adverse effects)</term><term>Oxazolone (pharmacology)</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Oxazolone</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Lymph Node Excision</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Lymphatic System</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Oxazolone</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lymphatic System</term><term>Lymphedema</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acute Disease</term><term>Animals</term><term>Female</term><term>Forelimb</term><term>Lymphography</term><term>Models, Animal</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Secondary lymphedema in humans is a common consequence of axillary lymph node dissection (ALND) to treat breast cancer. Remarkably, secondary lymphedema generally first appears following a delay of over a year and can be triggered suddenly by an inflammatory insult. However, it remains unclear why the apparently functional lymphatic system is unable to accommodate an inflammatory trigger. To provide mechanistic insight into the delayed and rapid secondary lymphedema initiation, we compared the ability of the ALND-recovered rat foreleg lymphatic system to prevent edema during an inflammatory challenge with that of the uninjured lymphatic system. At 73 days postsurgery, the forelegs of ALND(-)- and ALND(+)-sensitized rats were exposed to the proinflammatory agent oxazolone, which was found to reduce fluid drainage and increase skin thickness in both ALND(-) and ALND(+) forelegs (P < 0.05). However, drainage in the ALND-recovered forelegs was more severely impaired than ALND(-) forelegs, as visualized by indocyanine green lymphography and quantified by interstitial transport of fluid marker (P < 0.05). Although both ALND(+) and ALND(-) forelegs experienced significant inflammation-induced edema with the oxazolone exposure (P < 0.05), the peak tissue swelling in the ALND(+) group was significantly greater than that of the ALND(-) forelegs (arm area peaked at ∼13.4 vs. ∼5.7% swelling, respectively, P < 0.005; wrist diameter peaked at 9.7 vs. 2.2% swelling, respectively, P < 0.005). The findings demonstrate that outward recovery from ALND in the rat foreleg masks an ensuing chronic and latent lymphatic insufficiency, which reduces the ability of the foreleg lymphatic system to prevent edema during an acute inflammatory process.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22942182</PMID><DateCreated><Year>2012</Year><Month>11</Month><Day>05</Day></DateCreated><DateCompleted><Year>2013</Year><Month>01</Month><Day>14</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-1539</ISSN><JournalIssue CitedMedium="Internet"><Volume>303</Volume><Issue>9</Issue><PubDate><Year>2012</Year><Month>Nov</Month><Day>01</Day></PubDate></JournalIssue><Title>American journal of physiology. Heart and circulatory physiology</Title><ISOAbbreviation>Am. J. Physiol. Heart Circ. Physiol.</ISOAbbreviation></Journal><ArticleTitle>A chronic and latent lymphatic insufficiency follows recovery from acute lymphedema in the rat foreleg.</ArticleTitle><Pagination><MedlinePgn>H1107-13</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajpheart.00522.2012</ELocationID><Abstract><AbstractText>Secondary lymphedema in humans is a common consequence of axillary lymph node dissection (ALND) to treat breast cancer. Remarkably, secondary lymphedema generally first appears following a delay of over a year and can be triggered suddenly by an inflammatory insult. However, it remains unclear why the apparently functional lymphatic system is unable to accommodate an inflammatory trigger. To provide mechanistic insight into the delayed and rapid secondary lymphedema initiation, we compared the ability of the ALND-recovered rat foreleg lymphatic system to prevent edema during an inflammatory challenge with that of the uninjured lymphatic system. At 73 days postsurgery, the forelegs of ALND(-)- and ALND(+)-sensitized rats were exposed to the proinflammatory agent oxazolone, which was found to reduce fluid drainage and increase skin thickness in both ALND(-) and ALND(+) forelegs (P < 0.05). However, drainage in the ALND-recovered forelegs was more severely impaired than ALND(-) forelegs, as visualized by indocyanine green lymphography and quantified by interstitial transport of fluid marker (P < 0.05). Although both ALND(+) and ALND(-) forelegs experienced significant inflammation-induced edema with the oxazolone exposure (P < 0.05), the peak tissue swelling in the ALND(+) group was significantly greater than that of the ALND(-) forelegs (arm area peaked at ∼13.4 vs. ∼5.7% swelling, respectively, P < 0.005; wrist diameter peaked at 9.7 vs. 2.2% swelling, respectively, P < 0.005). The findings demonstrate that outward recovery from ALND in the rat foreleg masks an ensuing chronic and latent lymphatic insufficiency, which reduces the ability of the foreleg lymphatic system to prevent edema during an acute inflammatory process.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mendez</LastName><ForeName>Uziel</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Biomedical Engineering Department, Michigan Technological University, Houghton, Michigan 49931, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stroup</LastName><ForeName>Emily M</ForeName><Initials>EM</Initials></Author><Author ValidYN="Y"><LastName>Lynch</LastName><ForeName>Laura L</ForeName><Initials>LL</Initials></Author><Author ValidYN="Y"><LastName>Waller</LastName><ForeName>Anna B</ForeName><Initials>AB</Initials></Author><Author ValidYN="Y"><LastName>Goldman</LastName><ForeName>Jeremy</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R15-HL-093705</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21-AR053094</GrantID><Acronym>AR</Acronym><Agency>NIAMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21-HL-093568</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>08</Month><Day>31</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Heart Circ Physiol</MedlineTA><NlmUniqueID>100901228</NlmUniqueID><ISSNLinking>0363-6135</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>15646-46-5</RegistryNumber><NameOfSubstance UI="D010081">Oxazolone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Lymphology. 2007 Sep;40(3):122-6</RefSource><PMID Version="1">18062613</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2003 Mar;111(5):717-25</RefSource><PMID Version="1">12618526</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cancer. 1998 Dec 15;83(12 Suppl American):2798-802</RefSource><PMID Version="1">9874400</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Heart Circ Physiol. 2008 Mar;294(3):H1326-34</RefSource><PMID Version="1">18203849</PMID></CommentsCorrections><CommentsCorrections 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