Abstract
The RBC must exhibit a remarkable ability to undergo cellular deformation, since its diameter (8 pm in humans) far exceeds that of the capillaries (2 to 3 pm) I. In sepsis, RBC deformability may be altered by extrinsic (interactions with leukocytesand the release of oxygen free radicals) and intrinsic factors (the increased production of nitric oxidean increase in free intracellular calciumand a decrease in adenosine triphosphate). An increase in 2,3 diphosphoglycerate (2,3 DPG) concentration may also destabilize RBC membrane protein interactions. RBC deformability is also influenced by the behavior of different proteins of the RBC membrane. An important transmembrane protein is glycophorin A which is highly glycosylated in the RBC. The two sialic acid residues (N-acetyl-neuraminic acid; SA) of each of these oligosaccharides, account for 60% of the negative charge of the RBC. Because of the negative charge on the RBC membrane surface due to SA, in physiologic conditions, RBCs normally repel each other and do not aggregate. The importance of SA on RBC shape is demonstrated by the observation that neuraminidase-treated cells, which release their membrane SA content, undergo increased aggregation and display a reduced mean curvature. Decreases in RBC membrane SA content have been demonstrated in RBCs of patients with diabetes mellitusas well as in senescent RBCs. The decrease in SA may explain the increase of RBC aggregability observed in diabetes mellitusbut effects of SA on alterations of RBC shape remain controversial.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Mohandas N., Chasis JA. 1993. Red blood cell deformability, membraie material properties and shape: regulation by transmembrane, skeletal and cytosolic proteñs and lipids. Semin. Hematol. 30: 171–192.
Todd JC., Poulos ND., Davidson LW., Mollitt DL.1993. Role of the leukocyte inendotoxin-induced alterations of the red cell membrane. Am. Surg. 59:9–12.
Goode HF., Webster NR. 1993. Free radicals and antioxydants in sepsis. Crit. Care Med. 21: 1770–1776.
Graf J., Eichelbrönner O., Sibbald WJ. 1999 The red blood cell and nitric oxide. In: Vincent JL (ed). Yearbook of Intensive Care aid Emergency Medicine. Springier-Verlag, Berlin Heidelberg New York Tokyo. 465–475.
Todd JC., Mollitt DL. 1995. Effect of sepsis on erythrocyte intracellular calcium homeostasis. Crit. Care Med. 23: 459–465.
Marikovsky Y. 1996. The cytoskeleton in ATP-deplet;d erythrocytes: the effect of shape transformation. Mech. Ageing Dev. 86: 137–144.
Waugh RE. Effects of 2,3 diphosphoglycerate on the mechanical properties of erythrocyte membrane. Blood 1986; 68: 231–238.
Grebe R., Wolff H., Schmid-Schonbein H. 1988. Influence of red cell surface charge on redcell membrane curvature. Pflugers Arch. 413: 77–82.
Rogers ME., Williams DT., Niththyananthan R., Rampling MW., Heslop KE., Johnston DG. 1992. Decrease in erythrocyte glycophorin sialic acid content is associated with increased erythrocyte aggregation in human diabetes. Clin. Sci. 82: 309–13.
Baskurt OK., Gelmont D., Meiselman HJ. 1998. Red blood cell deformability ñ sepsis. Am. J. Respir. Crit. Care Med. 157: 421–427.
Astiz ME., DeGent GE., Lin RY., Rackow EC. 1995. Microvascular function and rheologic changes in hyperdynamic sepsis. Crit. Care Med. 23: 265–271.
Rolfes-Curl A., Ogden IL, Omann GM, Aminoff D. 1991. Flow cytometric analysis of hurnan erythrocytes: Possible identification of senescent RBC with fluorescently labeled wheat germ agglutinin. Exp. Gerontol. 26: 327–345.
ACCP/SCCM Consensus Conference. 1992. Definitions for sepsis and organ failure guidelines for the use of vasoactive therapies in sepsis. Crit. Care Med. 20: 864–874.
Lowry OH., Rosebrough JJ, Farr AL et al. 1951. Protein measurement with the folin phenol reagent. J. Biol. Chem. 193: 265–275.
Anumula KR. 1995. Rapid quantitative determination of sialic acids in glycoproteins by high-performance liquid chromatography with a sensitive fluorescence detection. Anal Biochem. 230: 24–30.
Gutowski KA, Hudson JL., Aminoff D. 1991. Flow cytometric analysis of human erythrocytes: I. Probed with lectins and immunoglobulins. Exp. Gerontol. 26: 315–326.
Hinshaw LB. 1996. Sepsis/septic shock: participation of the microcirculation: an abbreviated review. Crit. Care Med. 24: 1072–1078.
Gabay C., Kushner I. 1999. Acute-phase proteins and other systemic responses to inflammmation. N.Engl.J. Med. 340: 448–454.
Simchon S., Jan KM., Chien S. 1988. Studies on sequestration of neuraminidase-treated red blood cells.Am. J. Physiol. 254: H 1167- H 1171
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2003 Springer Science+Business Media New York
About this chapter
Cite this chapter
Piagnerelli, M., Vincent, JL., Boudjeltia, K.Z., Brohee, D., Vanhaeverbeek, M. (2003). Modifications of Red Blood Cell Shape and Glycoproteins Membrane Content in Septic Patients. In: Wilson, D.F., Evans, S.M., Biaglow, J., Pastuszko, A. (eds) Oxygen Transport To Tissue XXIII. Advances in Experimental Medicine and Biology, vol 510. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0205-0_18
Download citation
DOI: https://doi.org/10.1007/978-1-4615-0205-0_18
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-4964-8
Online ISBN: 978-1-4615-0205-0
eBook Packages: Springer Book Archive