Linked Life Data

7247737

Source:http://linkedlifedata.com/resource/pubmed/id/7247737

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1981-8-10
pubmed:abstractText
Changes of arterial wall lipid and connective tissue components were studied under various regression regimes on experimental high fat-cholesterol diet induced atherosclerosis in non-human primates. Levels of plasma lipids and aorta tissue lipids were closely related, while an inverse relationship between plasma cholesterol levels was noted with the ratio of aorta tissue free/ester cholesterol. Although the total content of glycosaminoglycan increased slightly with increasing disease, changes of individual glycosaminoglycans were most closely related to the severity of aorta atherosclerosis associated with both induction and regression of disease. With increasing atherosclerosis hyaluronic acid tended to decrease, while chondroitin sulfates decreased. Heparan sulfate decreased considerably with increasing severity of atherosclerosis. Consequently, regression regimens reducing the severity reversed the glycosominoglycan changes. Withdrawal of the dietary stimulus and cholestryamine produced the greatest reversal of atherosclerosis. In contrast, D-thyroxine treatment resulted in severe aorta atherosclerosis comparable to controls receiving no treatment. The effectiveness of regression depends on favorably altering plasma lipids but without adversely affecting the arterial wall structural elements.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0098-6127
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
44-58
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Chemical changes in the arterial wall during regression of atherosclerosis in monkeys.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.