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 The relation between health and

The relation between health and the viscosity of your blood.

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

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=15829825&itool=iconabstr&query_hl=2&itool=pubmed_DocSum

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.

 

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=15553798&itool=iconabstr&query_hl=2&itool=pubmed_DocSum

 

BACKGROUND: Blood viscosity is correlated with cerebral blood flow and cardiac output, and increased viscosity may increase the risk of thrombosis or thromboembolic events.

 

 

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=15296241&itool=iconabstr&query_hl=2&itool=pubmed_DocSum

 

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

Evidence of endothelial dysfunction in patients with functionally univentricular physiology before completion of the Fontan operation