Role of the altered transmural permeability in the pathomechanism of arteriosclerosis. History of arteriosclerosis theories. Role of the altered permeability in experimental arteriosclerosis models.
Identifieur interne : 006499 ( PubMed/Corpus ); précédent : 006498; suivant : 006500Role of the altered transmural permeability in the pathomechanism of arteriosclerosis. History of arteriosclerosis theories. Role of the altered permeability in experimental arteriosclerosis models.
Auteurs : H. Jellinek ; Z. DetreSource :
- Pathology, research and practice [ 0344-0338 ] ; 1986.
English descriptors
- KwdEn :
- MESH :
- complications : Hypertension, Hypoxia, Lymphedema.
- etiology : Arteriosclerosis.
- history : Arteriosclerosis.
- pathology : Arteriosclerosis.
- Animals, Capillary Permeability, Disease Models, Animal, History, 20th Century, Humans, Models, Cardiovascular.
Abstract
After presenting an overview on classification and history of arteriosclerosis theories, the physiological factors involved in the transmural permeability of the arteries are discussed in detail. The development and characteristic features of the altered transmural permeability were studied in various experimental models such as in rat's hypercholesterolemia, local aortic hypoxia, lymphedema of the vascular wall and in hypertension. Results appear to show that alterations in permeability invariably developed in all of the pathological conditions examined, they were transient in nature and preceded the onset of intimal proliferation(s). The disturbance of transmural permeability might be the common pathologic clue which initiates uniform vascular responses to injuries produced by a variety of noxious stimuli. The possible role of the altered transmural permeability in the induction of smooth muscle cell proliferation is also discussed and evidence is provided that after withdrawal of stimulus for vascular injury intimal proliferation will not develop despite the manifest disorders in permeability.
PubMed: 3550747
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pubmed:3550747Le document en format XML
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History of arteriosclerosis theories. Role of the altered permeability in experimental arteriosclerosis models.</title><author><name sortKey="Jellinek, H" sort="Jellinek, H" uniqKey="Jellinek H" first="H" last="Jellinek">H. Jellinek</name></author><author><name sortKey="Detre, Z" sort="Detre, Z" uniqKey="Detre Z" first="Z" last="Detre">Z. Detre</name></author></analytic><series><title level="j">Pathology, research and practice</title><idno type="ISSN">0344-0338</idno><imprint><date when="1986" type="published">1986</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Arteriosclerosis (etiology)</term><term>Arteriosclerosis (history)</term><term>Arteriosclerosis (pathology)</term><term>Capillary Permeability</term><term>Disease Models, Animal</term><term>History, 20th Century</term><term>Humans</term><term>Hypertension (complications)</term><term>Hypoxia (complications)</term><term>Lymphedema (complications)</term><term>Models, Cardiovascular</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Hypertension</term><term>Hypoxia</term><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Arteriosclerosis</term></keywords><keywords scheme="MESH" qualifier="history" xml:lang="en"><term>Arteriosclerosis</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Arteriosclerosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Capillary Permeability</term><term>Disease Models, Animal</term><term>History, 20th Century</term><term>Humans</term><term>Models, Cardiovascular</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">After presenting an overview on classification and history of arteriosclerosis theories, the physiological factors involved in the transmural permeability of the arteries are discussed in detail. The development and characteristic features of the altered transmural permeability were studied in various experimental models such as in rat's hypercholesterolemia, local aortic hypoxia, lymphedema of the vascular wall and in hypertension. Results appear to show that alterations in permeability invariably developed in all of the pathological conditions examined, they were transient in nature and preceded the onset of intimal proliferation(s). The disturbance of transmural permeability might be the common pathologic clue which initiates uniform vascular responses to injuries produced by a variety of noxious stimuli. The possible role of the altered transmural permeability in the induction of smooth muscle cell proliferation is also discussed and evidence is provided that after withdrawal of stimulus for vascular injury intimal proliferation will not develop despite the manifest disorders in permeability.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">3550747</PMID><DateCreated><Year>1987</Year><Month>05</Month><Day>06</Day></DateCreated><DateCompleted><Year>1987</Year><Month>05</Month><Day>06</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>23</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0344-0338</ISSN><JournalIssue CitedMedium="Print"><Volume>181</Volume><Issue>6</Issue><PubDate><Year>1986</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Pathology, research and practice</Title><ISOAbbreviation>Pathol. Res. Pract.</ISOAbbreviation></Journal><ArticleTitle>Role of the altered transmural permeability in the pathomechanism of arteriosclerosis. History of arteriosclerosis theories. Role of the altered permeability in experimental arteriosclerosis models.</ArticleTitle><Pagination><MedlinePgn>693-712</MedlinePgn></Pagination><Abstract><AbstractText>After presenting an overview on classification and history of arteriosclerosis theories, the physiological factors involved in the transmural permeability of the arteries are discussed in detail. The development and characteristic features of the altered transmural permeability were studied in various experimental models such as in rat's hypercholesterolemia, local aortic hypoxia, lymphedema of the vascular wall and in hypertension. Results appear to show that alterations in permeability invariably developed in all of the pathological conditions examined, they were transient in nature and preceded the onset of intimal proliferation(s). The disturbance of transmural permeability might be the common pathologic clue which initiates uniform vascular responses to injuries produced by a variety of noxious stimuli. The possible role of the altered transmural permeability in the induction of smooth muscle cell proliferation is also discussed and evidence is provided that after withdrawal of stimulus for vascular injury intimal proliferation will not develop despite the manifest disorders in permeability.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jellinek</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Detre</LastName><ForeName>Z</ForeName><Initials>Z</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016456">Historical Article</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Pathol Res Pract</MedlineTA><NlmUniqueID>7806109</NlmUniqueID><ISSNLinking>0344-0338</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CitationSubset>Q</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001161" MajorTopicYN="N">Arteriosclerosis</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000266" MajorTopicYN="Y">history</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002199" MajorTopicYN="Y">Capillary Permeability</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049673" MajorTopicYN="N">History, 20th Century</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006973" MajorTopicYN="N">Hypertension</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000860" MajorTopicYN="N">Hypoxia</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008955" MajorTopicYN="Y">Models, Cardiovascular</DescriptorName></MeshHeading></MeshHeadingList><NumberOfReferences>174</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1986</Year><Month>12</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1986</Year><Month>12</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1986</Year><Month>12</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">3550747</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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