Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1976-4-19
pubmed:abstractText
The purpose of this study was to determine if the fluid mechanical stresses associated with turbulent blood flow can contribute to the sickling process. Blood from seven patients with sickle cell disease was subjected to intermediate and high levels of turbulent flow in vitro. Turbulence was quantitated by hot film anemometry. Control samples showed 20 +/- 3% sickled cells. Cells subjected to intermediate levels of turbulent flow showed 26 +/- 4% sickling (P less than 0.01); and blood subjected to high intensities of turbulence showed 31 +/- 4% sickling (P less than 0.01). A quantitative count by electronmicroscopy, performed in one patient, showed polymerization of the hemoglobin indicative of sickling in more cells subjected to turbulence than in the control sample. A turbulence-reducing agent, polyethylene oxide, diminished the augmentation of the sickling process as it reduced turbulence at comparable Reynolds numbers. These results support the hypothesis that a deleterious effect upon hemoglobin SS erythrocytes may occur due to the mechanical stresses of turbulent flow. The agitation associated with turbulent flow presumably modifies the stabilizing factors of the intracellular colloidal solution of hemoglobin, thereby contributing to sol-gel transformation. Such hydrodynamic stresses may supplement the previously described factors which contribute to sickle cell crises.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-8987
pubmed:author
pubmed:issnType
Print
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
60-6
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1976
pubmed:articleTitle
Augmentation of sickling process due to turbulent blood flow.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.