Linked Life Data

6232395

Source:http://linkedlifedata.com/resource/pubmed/id/6232395

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1984-6-21
pubmed:abstractText
Using electron microscopy and cytochemical techniques we investigated structures which are associated with long-term hypertension and ageing in the myocardial cell of the rat. Lysosomes, demonstrated by acid phosphatase and aryl sulfatase activities, were found mainly in the perinuclear region in young rats. With age these organelles appeared with increasing frequency in other regions of the cell. Spontaneously hypertensive rats (SHR) showed an earlier apparent migration of lysosomes than did normotensive rats (WKY). Our observations indicate that lysosomes were closely associated with autophagic vacuoles, membrane swirls , translucent mitochondria, myelin figures and other structures linked with degenerative events. In the oldest SHR lysosomes, autolysosomes (autophagic vacuoles with lysosomal activity), and degenerative structures were observed in various regions of the myocardial cell. Peroxisomes, as demonstrated by catalase activity, did not seem to be affected by hypertension or age. A number of dense osmophilic structures did not react for any of the enzymes studied; these included myelin figures, mitochondrial inclusions and diffuse dense bodies. Our observations implicate both ageing and hypertension in the enhancement of lysosomes and their end products.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
227-37
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Cytochemistry of myocardial structures related to degenerative processes in spontaneously hypertensive and normotensive rats.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.