Linked Life Data

2809726

Source:http://linkedlifedata.com/resource/pubmed/id/2809726

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5 Pt 1
pubmed:dateCreated
1989-11-24
pubmed:abstractText
The role of the aging human erythrocyte in the mechanisms leading to cerebral vasospasm after subarachnoid hemorrhage was investigated using an in vitro model for the environment of the erythrocyte in a subarachnoid blood clot. It has long been suspected that, due to its potent vasoactivity, erythrocyte lysate provides the major vasoconstrictive input to cerebral arteries during vasospasm. Under the model conditions (incubation at 37 degrees C in an artificial cerebrospinal fluid), however, the rate of spontaneous hemolysis was quite slow (about 1%/day), becoming only somewhat more rapid after 4 days' incubation. The rate of hemolysis of aging erythrocytes was dramatically increased (500- to 1000-fold) by the addition of plasma proteins, but only after the erythrocytes had aged 2 to 3 days, or more. The mechanism of age-dependent, plasma-induced hemolysis of originally autologous erythrocytes is shown to involve activation of the plasma complement protein pathway, analogous to the mechanisms of innate immunity which lead to lysis of nonautologous cell types and activate the inflammatory response.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-3085
pubmed:author
pubmed:issnType
Print
pubmed:volume
71
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
718-26
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Immunological reaction against the aging human subarachnoid erythrocyte. A model for the onset of cerebral vasospasm after subarachnoid hemorrhage.
pubmed:affiliation
Laboratory for Cerebrovascular Biophysics, Massachusetts General Hospital, Boston.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.