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Page last updated: 2006-11-10. |
Author of this page: Wim
Vogelaar. |
Click on: Arthritis and the viscosity of blood
Click here
to see a long list with PUBMED articles that show what the viscosity of your
blood is doing in your body.
Of some of those articles the URL is mentioned here. The URL is followed by a few sentences coming from that article.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16614465&itool=iconabstr&query_hl=2&itool=pubmed_docsum
CONCLUSIONS:
Patients with kidney disease have increased blood viscosity at all shear
rates. This may be related to changes in RBC shape and decreased
deformability in patients with kidney disease, independent of HD- or
DM-status. This may have implications for strategies to treat anemia in
these patients.
BACKGROUND:
Anemia of renal failure is primarily a problem of decreased RBC production
due to erythropoietin deficiency. RBC survival is also reduced, perhaps
due to decreased RBC deformability. This study measured blood viscosity
over a range of shear rates in erythropoietin-treated patients on
hemodialysis (HD), and compared the findings to matched patients with
chronic renal insufficiency (CRI) and healthy controls. METHODS: Four
groups (control, CRI, non-diabetic HD, and diabetic HD) of 9 matched
subjects were recruited. Blood viscosity was measured using a cone-plate
viscometer over a variety of shear rates (11 to 225 s(-1)). RESULTS:
Control subjects had lower viscosity values throughout all shear rates
when compared to the 3 renal disease groups (P value=0.039). A trend was
observed to higher levels of renal function being associated with
decreased blood viscosity in patients with CRI. CONCLUSIONS: Patients with
kidney disease have increased blood viscosity at all shear rates. This may
be related to changes in RBC shape and decreased deformability in patients
with kidney disease, independent of HD- or DM-status. This may have
implications for strategies to treat anemia in these patients.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16151255&itool=iconabstr&query_hl=2&itool=pubmed_DocSum
Many
studies have shown that diabetes mellitus is associated with increased
whole and blood viscosity and decreased erythrocyte deformability. It has
been suggested that these abnormalities in blood rheology may play a
causative role in the pathogenesis of diabetic vascular complications.
However, less is known about the content and quality of membrane proteins
which may contribute to abnormalities in membrane dynamic and decreased
erythrocyte deformability.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16040719&itool=iconabstr&query_hl=2&itool=pubmed_DocSum
The
apparent viscosity of blood in glass tubes declines with decreasing
diameter (Fahraeus-Lindqvist effect) and exhibits a distinctive minimum at
6-7 microm. However, flow resistance in vivo in small vessels is
substantially higher than predicted by in vitro viscosity data. The
presence of a thick endothelial surface layer (ESL) has been proposed as
the primary cause for this discrepancy. Here, a physical model is proposed
for microvascular flow resistance as a function of vessel diameter and
hematocrit in vivo; it combines in vitro blood viscosity with effects of a
diameter-dependent ESL. The model was developed on the basis of flow
distributions observed in three microvascular networks in the rat
mesentery with 392, 546, and 383 vessel segments, for which vessel
diameters, network architecture, flow velocity, and hematocrit were
determined by intravital microscopy. A previously described hemodynamic
simulation was used to predict the distributions of flow and hematocrit
from the assumed model for effective blood viscosity.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16015032&itool=iconabstr&query_hl=2&itool=pubmed_DocSum
This
supports the pathophysiological concept that sleep apnea is a cardiovascular risk factor. Copyright (c) 2005
S. Karger AG, Basel.
CONCLUSIONS:
Patients with OSA
have elevated morning fibrinogen levels and a higher
plasma viscosity, which correlate positively with indices of sleep
apnea severity. These changes in blood rheology are independent of
cardiovascular risk factors, and therefore, might be specific mechanisms
of OSA. This supports the pathophysiological concept that sleep apnea is a
cardiovascular risk factor. Copyright (c) 2005 S. Karger AG, Basel.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16036496&itool=iconabstr&query_hl=2&itool=pubmed_DocSum
We
studied effects of mental stress on whole-blood viscosity (WBV) and blood
pressure (BP), and relations between WBV and autonomic nervous system
activity and insulin sensitivity.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=15977847&itool=iconabstr&query_hl=2&itool=pubmed_DocSum
A
study of biological fluids by ultrasound coagulography
http://vascular.stanford.edu/vasc_bio_lab/research/wall_shear.html
Arteries
enlarge in response to high shear stress Low
plasma viscosity was associated with a low WSS, which implies a
contradiction, because both high WSS and low plasma viscosity are thought
to be indicators for a healthy system. CONCLUSIONS:
Flow and diameter changes have significant influence on wall shear stress
values; the same is true for the viscosity, but to a lesser extent. BACKGROUND:
Blood viscosity is correlated with cerebral blood flow and cardiac output,
and increased viscosity may increase the risk of thrombosis or
thromboembolic events. To
clarify the relationship of the intensity of acute exercise to sudden
cardiac death, we examined the effects of short-term heavy and light
exercise on whole blood viscosity. Nine healthy sedentary male volunteers
performed ten minutes of heavy (more than 95% of maximum oxygen
consumption) or light (60% to 65% of maximum oxygen consumption) exercise.
Blood samples were obtained before, immediately after, and one hour after
exercise. The whole blood viscosity was immediately examined with an
oscillation-type viscometer and was found to increase significantly after
exercise and subsequently return to baseline levels within one hour after
exercise. The whole blood viscosity increased by a similar degree after
heavy or light exercise. Therefore, our results suggest that there is a
similar risk of sudden cardiac death, due to increased whole blood viscosity,
after short-term heavy or light exercise. http://www.ingentaconnect.com/content/gmed/city/2005/00000015/00000001/art00006
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