Blood viscosity in multiple sclerosis.

G W Blair; R H Matchett

doi:10.1136/jnnp.35.5.730

Home/Archive/PubMed

PubMed · 5084142

Blood viscosity in multiple sclerosis.

G W Blair·R H Matchett

View original source ↗Export metadata ↓

Abstract

Native blood from healthy subjects and from some pathological cases showed a fall in viscosity after the first passage through a stainless steel capillary viscometer in 97% of tests. Fortyfive blood samples from 27 active multiple sclerosis patients were tested. Blood from 19 of these patients showed no fall in viscosity.

Explore related subjects

Blood Viscosity Humans Multiple Sclerosis Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

G W Blair, R H Matchett. 1972. Blood viscosity in multiple sclerosis.. https://doi.org/10.1136/jnnp.35.5.730

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

Fluid mechanical and physicochemical modeling interprets hypertension to be capable of inducing secondary complications.

The relationship of hypertensives and many pathological syndromes still remains unclear. A mathematical model in terms of the fluid mechanics and physicochemical analyses is established to correlate the plasma viscosity, the shear stress and the rate of shear in blood stream with the ligand-receptor dissociation constant. This model has arrived at the conclusive results that high viscosity, high rate of shear created in the blood streams, and the peripheral resistance may act as important preceding factors to induce a serial subsequent pathological clinical manifestations. High viscosity may interfere with the ligand-receptor combination, in contrast, high rate of shear may knock the ligand (s) off the existing ligand-receptor complex, while elevation of peripheral resistance may slow down the blood flow rate, resulting in a diminished dissociation of ligand-receptor complex. This model has successfully interpreted the possible cause of some post-hypertensive abnormal outcome manifestations involving obstructive and degenerative stenosis (such as renal artery stenosis), growth retardation, blood vessel detriment, coarctation of aorta, coronary thrombotics, atherosclerosis, hyperinsulinemia, diabetes, obesity, hypothyroidism, infertility, and at the worst, carcinoma, etc.

Blood Viscosity↗

PubMed2006

The mechanism of the dextran-induced red blood cell aggregation.

In order to clarify the mechanism of dextran-induced aggregation, the effect of the ionic strength (I) on the minimal shear stress (tau(c)) required to rupture RBC doublets was studied for suspensions with the external media containing 76 and 298 kDa dextrans. At low and high ionic strengths, tau(c) increases with increasing I, whereas at intermediate I values, tau(c) versus I dependencies reveal a plateau step. The non-monotonous shape of these curves disagrees with the depletion model of RBC aggregation and is consistent with the predictions of the bridging mechanism. Literature reports point out that elastic behavior of dextran molecules in low and high I regions is fairly typical of Hookean springs and hence predict an increase in tau(c) with increasing I. A plateau step is accounted for by the enthalpic component of the dextran elasticity due to the shear-induced chair-boat transition of the dextran's glucopyranose rings. A longer plateau step for suspensions with a higher molecular weight dextran is explained by a larger contribution of the enthalpic component to the dextran elasticity. Thus, the results reported in this study provide evidence that RBC aggregation is caused by the formation of dextran bridges between the cells.

Blood Viscosity↗

PubMed2006

Changes in blood viscosity with the recombinant tissue plasminogen activator alteplase.

We measured whole blood viscosity to investigate the time course of the fibrinolytic activity of the recombinant tissue plasminogen activator alteplase. Changes in blood viscosity over time were determined using an oscillation-type viscometer at a shear rate of 400 to 500 per second. Blood viscosity initially increased with alteplase as in untreated blood, but then decreased, reflecting the fibrinolytic activity of generated plasmin. Blood viscosity subsequently stabilized at a level below the initial value owing to the dissolution of both fibrin and fibrinogen by alteplase. To our knowledge, the present study is the first to examine the time course of changes in BV during fibrin formation and degradation. The results indicated that the fibrinolyic agent alteplase might provide the additional benefit of increasing blood flow by lowering blood viscosity.

Blood Viscosity↗