Background: In carrying out their role of free radical scavenging, erythrocytes become damaged due to oxidation of membrane lipids and proteins. Such damage changes the morphology and rheological properties (erythrocyte aggregation, erythrocyte deformability and whole blood viscosity) of the erythrocytes. It has been shown that altered haemorheology leads to slowed coronary blood flow, resulting in altered microcirculation. Erythrocyte aggregates may form a thrombus at low shear stress. Vascular dysfunction is associated with metabolic syndrome and its components. In this context, the objective of our study was to demonstrate haemorheological abnormalities and decreased peripheral blood flow in metabolic syndrome and to associate abnormal blood rheological characteristics with chronic inflammation and oxidative stress in the same subjects. Materials and methods: 100 participants were recruited from a rural Australian town (Albury and Wodonga). Anthropometric measurements (blood pressure from arm, waist circumference, height and weight) and twenty mL of blood sample were obtained from the research participants. Blood pressure was also measured from the great toe of the research participants (to calculate toe brachial pressure index) using the Systoe method to assess the status of peripheral blood circulation. Whole blood viscosity, erythrocyte aggregation, erythrocyte deformability, erythrocyte morphology, lipid profile and blood sugar level were analysed. In addition, oxidative stress markers: erythrocyte reduced glutathione, superoxide dismutase and urinary isoprostanes; inflammatory markers high-sensitivity C-reactive protein; and thrombotic marker D-dimer were measured. Recruited participants were classified into two groups: with and without metabolic syndrome following the National Cholesterol Education Program Adult Treatment Panel III definition (Expert Panel on Detection Evaluation Treatment of High Blood Cholesterol in Adults, 2001). Data were analysed by IBM SPSS 20 software. Results: Whole blood viscosity (P-value <0.0005) and erythrocyte aggregation (P-value <0.0005) were higher whereas erythrocyte deformability (P-value <0.0005) was lower in participants with metabolic syndrome when compared to participants without metabolic syndrome. Morphologically abnormal erythrocytes (when viewed using scanning electron microscopy) were found to be significantly higher in metabolic syndrome compared to non metabolic syndrome group (P-values for: acanthocytes <0.0005, echinocytes 0.006 and stomatocytes 0.001). Altered haemorheology and abnormal erythrocyte morphology were significantly associated with chronic inflammation and oxidative stress in metabolic syndrome. Also, there was a significant reduction in peripheral blood flow (decreased toe brachial pressure index, P-value <0.0005) among metabolic syndrome participants. Conclusions: Haemorheological alterations and reduced peripheral blood flow were demonstrated in metabolic syndrome. Defective microcirculation due to altered haemorheology could be one of the several pathogenic mechanisms underlying complications of metabolic syndrome. Alterations of haemorheology in metabolic syndrome are probably due to the effect of chronic inflammation and oxidative stress. Free radicals and inflammatory molecules generated in increased concentration in metabolic syndrome seem to damage the erythrocyte changing its morphology and deformability which affect other haemorheological parameters. The negative effect of inflammatory and oxidant molecules seen in the cardiovascular system could be due to the resulting altered haemorheology. Altered haemorheology could be the bridge that connects metabolic syndrome with cardiovascular diseases.
|Qualification||Doctor of Philosophy|
|Award date||01 Feb 2015|
|Place of Publication||Australia|
|Publication status||Published - 2015|