12 research outputs found

    Physical properties of blood are altered in young and lean women with polycystic ovary syndrome

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    Classic features of polycystic ovary syndrome (PCOS) include derangement of metabolic and cardiovascular health, and vascular dysfunction is commonly reported. These comorbidities indicate impaired blood flow; however, other than limited reports of increased plasma viscosity, surprisingly little is known regarding the physical properties of blood in PCOS. We aimed to investigate whether haemorheology was impaired in women with PCOS. We thus measured a comprehensive haemorheological profile, in a case-control design, of lean women with PCOS and age-matched healthy controls. A clinical examination determined similar cardiovascular risk for the two groups. Whole blood and plasma viscosity was measured using a cone-plate viscometer. The magnitude and rate of red blood cell (RBC) aggregation was determined using a light-transmission aggregometer, and the degree of RBC deformability was measured via laser-diffraction ektacytometry. Plasma viscosity was significantly increased in women with PCOS. Blood viscosity was also increased for PCOS at lower-to-moderate shear rates in both native and standardised haematocrit samples. The magnitude of RBC aggregation–a primary determinant of low-shear blood viscosity–was significantly increased in PCOS at native and 0.4 L·L(-1) haematocrit. No difference was detected between PCOS and CON groups for RBC deformability measurements. A novel measure indicating the effectiveness of oxygen transport by RBC (i.e., the haematocrit-to-viscosity ratio; HVR) was decreased at all shear rates in women with PCOS. In a group of young and lean women with PCOS with an unremarkable cardiovascular risk profile based on clinical data, significant haemorheological impairment was observed. The degree of haemorheological derangement observed in the present study reflects that of overt chronic disease, and provides an avenue for future therapeutic intervention in PCOS

    Acute Free-Iron Exposure Does Not Explain the Impaired Haemorheology Associated with Haemochromatosis.

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    Given the severity of the current imbalance between blood donor supply and recipient demand, discarded blood drawn from the routine venesections of haemochromatosis (HFE-HH) patients may serve as a valuable alternative source for blood banks and transfusion. We investigated whether functional or biochemical differences existed between HFE-HH and control blood samples, with particular focus upon the haemorheological properties, to investigate the viability of venesected blood being subsequently harvested for blood products.Blood samples were collected from HFE-HH patients undergoing venesection treatment (n = 19) and healthy volunteers (n = 8). Moreover, a second experiment investigated the effects of a dose-response of iron (0, 40, 80, 320 mM FeCl3) on haemorheology in healthy blood samples (n = 7). Dependent variables included basic haematology, iron status, haematocrit, red blood cell (RBC) aggregation (native and standardised haematocrit) and "aggregability" (RBC tendency to aggregate in a standard aggregating medium; 0.4 L/L haematocrit in a Dx70), and RBC deformability.Indices of RBC deformability were significantly decreased for HFE-HH when compared with healthy controls: RBC deformability was significantly decreased at 1-7 Pa (p < 0.05), and the shear stress required for half maximal deformability was significantly increased (p < 0.05) for HFE-HH. RBC aggregation in plasma was significantly increased (p < 0.001) for HFE-HH, although when RBC were suspended in plasma-free Dx70 no differences were detected. No differences in RBC deformability or RBC aggregation/aggregability were detected when healthy RBC were incubated with varying dose of FeCl3.HFE-HH impairs the haemorheological properties of blood; however, RBC aggregability was similar between HFE-HH and controls when cells were suspended in a plasma-free medium, indicating that plasma factor(s) may explain the altered haemorheology in HFE-HH patients. Acute exposure to elevated iron levels does not appear (in isolation) to account for these differences. Further consideration is required prior to utilising routine venesection blood for harvesting RBC concentrates due to the potential risk of microvascular disorders arising from impaired haemorheology

    Aggregation of RBC suspensions in autologous plasma following incubation with various concentration of FeCl<sub>3</sub>.

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    <p>Incubation with FeCl<sub>3</sub> did not influence the RBC aggregation at stasis (M<sub>0</sub>; Panel A) or at low-shear (M<sub>1</sub>; Panel B).</p

    Red cell aggregation for haemochromatosis (HFE-HH) patients and healthy controls (Con) measured in plasma suspensions at native and a standardised (0.4 L/L) haematocrit, and red cell aggregability in a standard aggregating medium (Dx70).

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    <p>Red cell aggregation was increased for HFE-HH when compared with Con while at stasis (“M<sub>0</sub>”; Panel A) at native and standardised haematocrit. The same observation was made for aggregation measures at low-shear (“M<sub>1</sub>”; Panel B). Red cell aggregability was not different between groups at stasis or low-shear. ***, HFE-HH significantly increased compared with Con, p < 0.001.</p

    Red cell deformability (Elongation Index; Panel A) was decreased at discrete shear stresses for haemochromatosis (HFE-HH) when compared with healthy controls (CON).

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    <p>Maximal Elongation Index (EI<sub>max</sub>) was not different between groups (Panel B); however, the shear stress required for half-maximal elongation index (SS<sub>1/2</sub>) was significantly increased for HFE-HH (Panel C). *, p < 0.05. **, p < 0.01.</p

    The Elongation Index (EI) of RBC in autologous plasma at varying shear stresses (Panel A) following an incubation with varying concentration of FeCl<sub>3</sub> (0, 40, 80, 320 uM).

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    <p>The varied iron incubated conditions did not influence the maximal EI (EI<sub>max</sub>; Panel B) or the amount of shear stress required for half maximal EI (SS<sub>half</sub>; Panel C).</p
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