Linked Life Data

2345534

Source:http://linkedlifedata.com/resource/pubmed/id/2345534

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1990-7-3
pubmed:abstractText
It is hypothesized that a cause of AMS could be vascular occlusion due to hemostatic plugs formed by DIPA (decompression-inducible platelet aggregation). Ex vivo experiments led to the current hypothesis that the rate of fibrin polymerization is accelerated by decompression and decelerated by compression. When experimental pressure is 253 torr (as at the top of Mt. Everest): (1) DIPA takes place independently of PO2; (2) ex vivo DIPA can be inhibited by menthol, thymol, piracetam and pentoxifylline. The experimental design was based on the premise that oppositely charged amino acid residues of adhesive site(s) are juxtaposed. Interaction of oppositely charged residues results in relaxation of electric constriction which causes the volume of the solution to increase. Because of the pressure-volume relationship, decompression alone can induce platelet aggregation. It is concluded that DIPA can be prevented and/or reversed by recompression, and by agents with a large electric dipole moment. It is suggested that the data presented here could be useful for DIPA investigations in vivo toward the prevention and/or alleviation of AMS.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0306-9877
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
189-95
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
AMS (acute mountain sickness), a vascular occlusive disease.
pubmed:affiliation
Laboratory of Physical Biology, NIAMS, NIH, Bethesda, Maryland 20892.
pubmed:publicationType
Journal Article