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Acta Physiologica Congress

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Acta Physiologica 2012; Volume 206, Supplement 692
The 63rd National Congress of the Italian Physiological Society
9/21/2012-9/23/2012
Verona, Italy


MORPHOLOGICAL AND RHEOLOGICAL PROPERTIES OF HUMAN RED BLOOD CELLS UNDER OXIDATIVE INSULT
Abstract number: P4.24

MAZZULLA1 S, SCHELLA1 A, GABRIELE2 D, BALDINO2 N, SESTI1 S, PERROTTA3 E, COSTABILE4 A, DE CINDIO2 B

1Dept Cell Biology, Calabria Univ., Italy
2Dept Chem., Eng. and Materials, Calabria Univ., Italy
3Dept Ecology, Calabria Univ., Italy
4Ass., Vol., Ital., Sangue (A.V.I.S.), Municipal Section, Cosenza, Italy

Aim: The aim of this study was to find a correlation between the rheological properties and morphological changes of Red Blood Cells (RBCs) during the oxidative injury induced by 2,2-azo-bis (2-amidinopropane) dihydrochloride (AAPH) in blood donors with borderline level of hyperlipidemia compared with a control group.

Methods: Haemolysis was evaluated spectrophotometrically. The RBCs deformability index (elasticity) was determined by creep tests performed on a Dynamic Stress Rheometer (DSR-500) and morphological changes were observed with an DSM 940 scanning electron microscope.

Results: The total elasticity values suggest a RBCs deformability reduction in the borderline group compare to control group causing an enhancement of the solid-like behaviour of RBCs suspensions. The deformability reduction is associated to a decreased globular resistance and acanthocytes formation in a AAPH exposure time-dependent manner. The increased viscosity observed in the control group is a typical trend of suspensions of materials in which the suspended particles have a greater rigidity, while in the borderline group probably rouleaux and RBCs lysis induce a compensatory effect on viscoelastic behavior.

Conclusions: RBCs shown shape changes under oxidative injury and can be permanently altered by excessive exposure affecting deformability in a time dependent-manner rather than aggregability in subjects with borderline level of hyperlipidemia.

To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 692 :P4.24

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