AUTHOR COPY Clinical Hemorheology and Microcirculation 56 (2014) 41–46 DOI 10.3233/CH-121654 IOS Press 41 Red blood cell deformability is very slightly decreased in erythropoietin deficient mice Aur´ elien Pichon a,∗ , Yann Lamarre b , Nicolas Voituron a , Dominique Marchant a , Jos´ e Vilar c , Jean-Paul Richalet a and Philippe Connes b a Universit´ e Paris 13, Sorbonne Paris Cit´ e, Laboratoire «R´ eponses cellulaires et fonctionnelles ` a l’hypoxie» EA2363, Bobigny, France b UMR Inserm S 665, Universit´ e des Antilles et de la Guyane/Universit´ e Paris Diderot, Hˆ opital Ricou, CHU de Pointe-` a-Pitre, Pointe-` a-Pitre, Guadeloupe c Inserm U970, Centre de Recherche Cardiovasculaire, Hˆ opital Europ´ een Georges Pompidou, Universit´ e Paris 5, Paris, France Abstract. The present study compared the hemorheological properties between Epo-TAg h mice (a model of erythropoietin deficient mice) and wild-type (WT) control mice. Blood viscosity was determined at several shear rates using a cone-plate viscometer at native and adjusted hematocrit (i.e. 40%). Red blood cell (RBC) deformability was measured by ecktacytometry at several shear stresses and RBC aggregation properties by backscattered technique at adjusted hematocrit (i.e. 40%). Epo- TAg h mice had severe anemia (very low hematocrit), decreased blood viscosity at native hematocrit and slightly reduced RBC deformability at high shear stresses in comparison with WT mice. Blood viscosity at adjusted hematocrit (i.e. 40%) was not different between WT and Epo-TAg h mice. RBC aggregation did not differ between the two mice models. These findings suggest a role of erythropoietin in the regulation of RBC deformability. Keywords: Erythropoietin, hemorheology, anemia 1. Introduction Erythropoietin (EPO) is known as a key-regulator of erythropoiesis stimulating proliferation, differen- tiation, and survival growth of erythroid precursor resulting in the increased production of red blood cells (RBC) [10]. In altitude or simulated hypoxia, EPO increases and causes a rise of RBC counts, hematocrit and blood viscosity [15]. In contrast, EPO deficiency such as in chronic kidney disease (CKD) may result in severe anemia and very low blood viscosity [14]. Decreased RBC deformability and survival have been postulated to contribute to the anemia and progressive cardiovascular impairment in CKD patients [11, 14]. The results on the effects of EPO therapy on RBC rheology in animals or various diseases are incon- sistent with studies demonstrating a decrease [6, 11], a lack of change [11, 14] or an improvement [5, 8, 17] of RBC deformability. To gain insight into the effects of EPO on blood rheology, we compared the hemorheological properties between Epo-TAg h mice (a model of EPO deficient mice) and wild-type (WT) control mice. The study of the hemorheological profile of Epo-TAg h mice should provide important information regarding the likeness, or not, of RBC rheology with humans with CKD disease. ∗ Corresponding author: Aur´ elien Pichon, PhD, Universit´ e Paris 13, Laboratoire «R´ eponses cellulaires et fonctionnelles ` a l’hypoxie» EA2363, Bobigny, France. Tel.: +33 148387632; Fax: +33 148388924; E-mail: aurelien.pichon@orange.fr. 1386-0291/14/$27.50 © 2014 – IOS Press and the authors. All rights reserved