Erythrocyte deformability in diabetes and erythrocyte membrane lipid composition

Garnier, M.; Attali, Jean-Raymond; Valensi, P.; Delatour-Hanss, E.; Gaudey, F.; Koutsouris, D.

doi:10.1016/0026-0495(90)90121-r

Cited by 75 publications

(52 citation statements)

References 27 publications

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“…Previous studies that investigated erythrocyte deformability in diabetic patients 3,[11][12][13][14][15][16][17][18][19][20][21][22][23] yielded conflicting results. In most of these studies, only some aspects of RBC deformability were studied, and the investigations included only a small number of diabetic patients, with or without microcirculatory decompensation as evidenced by end-organ involvement.…”

mentioning

confidence: 95%

Low-Frequency Submicron Fluctuations of Red Blood Cells in Diabetic Retinopathy

Alster

Loewenstein²,

Levin³

et al. 1998

Arch Ophthalmol

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mentioning

confidence: 95%

Low-Frequency Submicron Fluctuations of Red Blood Cells in Diabetic Retinopathy

Alster

Loewenstein²,

Levin³

et al. 1998

Arch Ophthalmol

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“…Thus, the efficacy of pentoxyfilline may be pronounced in diabetic patients, especially in light of the fact that it is recognized that this patient group has now been reported to have less deformable erythrocytes 22 and to release low amounts of ATP 11 compared to healthy, nondiabetic patients.…”

Section: Discussionmentioning

confidence: 99%

Red Blood Cell Stimulation of Platelet Nitric Oxide Production Indicated by Quantitative Monitoring of the Communication between Cells in the Bloodstream

Carroll

Karunarathne

et al. 2007

Anal. Chem.

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ATP is a recognized stimulus of nitric oxide synthase and is released from red blood cells (RBCs) upon deformation. The objective of this work is to demonstrate that RBCs stimulate nitric oxide production in platelets by employing a continuous flow analysis system in which the stream contains both RBCs and platelets. Here, two drugs known to improve blood flow in vivo (pentoxyfilline and iloprost) are shown to increase both the release of RBC-derived ATP and the production of platelet-derived NO. A flowbased chemiluminescence assay (in vitro) was employed to quantitatively determine the amount of ATP released from erythrocytes subjected to flow-induced deformation. Prior to being subjected to flow, erythrocytes were incubated in the absence or presence of 4.8 µM pentoxyfilline or 80 nM iloprost. Erythrocytes obtained from rabbits (n ) 22) that were subjected to flow released 239 ( 29 nM ATP. When treated with pentoxyfilline, the ATP released from the flowing RBCs increased to 450 ( 94 nM ATP. An increase in RBC-derived ATP was also measured for iloprost-incubated RBCs in flow (362 ( 45 nM ATP). Importantly, platelets that were loaded with diaminofluorofluorescein diacetate, an intracellular fluorescence probe for NO, exhibited increases in fluorescence intensity by 16% in the presence of RBCs treated with pentoxyfilline and a 10% increase when treated with iloprost. When the ATP release from the RBCs was inhibited with glybenclamide, the platelet fluorescence intensity decreased by 25 and 51% for RBCs incubated with pentoxyfilline and iloprost, respectively. In an experiment not involving the RBC, inhibition of the P2x receptor on the platelets (an ATP receptor) resulted in no increase in platelet NO production, suggesting that the NO production in the activated platelet is due to ATP.In addition to its well-known ability as a vasodilator, NO is also able to inhibit platelet activation and aggregation. Platelets have also been shown to produce NO upon activation. 1 Freedman et al. simultaneously measured NO production and aggregation of platelets upon activation with ATP. 2 These authors placed an electrode for NO into the cell of an aggregometer in order to simultaneously monitor the NO release from platelets and the aggregation of the platelets, thus demonstrating that NO was produced and released by these cells upon activation. From these studies, the authors concluded that NO released by the platelets was key to preventing further platelet recruitment to the activated platelets, but only mildly prevented their adhesion to an endothelium.In question concerning the production and release of plateletderived NO is the mechanism by which the NO production is stimulated. For example, ATP is a recognized stimulus of nitric oxide synthase (NOS) and subsequent production of platelet NO; moreover, it is also known that ATP is released from platelets upon activation. 3 However, it has not been established if ATP released from activated platelets has the ability to stimulate the production of NO in platelets. Here, res...

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“…The relative amounts of phospholipids and cholesterol are responsible for the fluid properties of erythrocyte membrane. Increase in the cholesterol content of the erythrocyte membrane alters the membrane behavior making it rigid (12,(14)(15)(16)(17)(18).The erythrocytes are devoid of many sub-cellular organelles, including ribosomes, hence erythrocytes cannot synthesis the cellular as well as membrane components and has to be dependent on the media i.e., plasma for these components. Therefore, the membrane properties of erythrocytes are dependent on plasma lipid components, specifically, the cholesterol.…”

Section: Introductionmentioning

confidence: 99%