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Circulating endothelial progenitor cells in adults with sickle cell disease

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      Circulating endothelial progenitor cells, vascular function, and cardiovascular risk.

      Cardiovascular risk factors contribute to atherogenesis by inducing endothelial-cell injury and dysfunction. We hypothesized that endothelial progenitor cells derived from bone marrow have a role in ongoing endothelial repair and that impaired mobilization or depletion of these cells contributes to endothelial dysfunction and cardiovascular disease progression. We measured the number of colony-forming units of endothelial progenitor cells in peripheral-blood samples from 45 men (mean [+/-SE] age, 50+/-2 years). The subjects had various degrees of cardiovascular risk but no history of cardiovascular disease. Endothelium-dependent and endothelium-independent function was assessed by high-resolution ultrasonography of the brachial artery. We observed a strong correlation between the number of circulating endothelial progenitor cells and the subjects' combined Framingham risk factor score (r=-0.47, P=0.001). Measurement of flow-mediated brachial-artery reactivity also revealed a significant relation between endothelial function and the number of progenitor cells (r=0.59, P<0.001). Indeed, the levels of circulating endothelial progenitor cells were a better predictor of vascular reactivity than was the presence or absence of conventional risk factors. In addition, endothelial progenitor cells from subjects at high risk for cardiovascular events had higher rates of in vitro senescence than cells from subjects at low risk. In healthy men, levels of endothelial progenitor cells may be a surrogate biologic marker for vascular function and cumulative cardiovascular risk. These findings suggest that endothelial injury in the absence of sufficient circulating progenitor cells may affect the progression of cardiovascular disease. Copyright 2003 Massachusetts Medical Society
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        Pulmonary complications of sickle cell disease.

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          Endothelial dysfunction in patients with sickle cell disease is related to selective impairment of shear stress-mediated vasodilation.

          Interactions between the endothelium and erythrocytes may contribute to the vascular complications of sickle cell disease (SCD). Endothelium-derived nitric oxide (NO) plays a major role in the regulation of vasomotor tone in response to wall shear stress (WSS) variations and pharmacologic stimuli. However, little is known about endothelial NO production in patients with steady-state SCD. We investigated endothelial NO production in response to flow or vasoactive agonists in 16 homozygous patients with steady-state SCD and 15 controls. Flow-mediated dilation (FMD), arterial diameter changes in response to 100% oxygen inhalation, blood viscosity, and calculated WSS were determined in all patients and controls. At baseline, WSS was higher in SCD patients than in controls, whereas arterial diameter was similar. In patients with SCD, FMD was impaired (1.73% +/- 0.44% vs 3.97% +/- 0.24% in the controls, P <.001) and vasoconstriction in response to 100% oxygen was abolished. Using venous occlusion plethysmography, forearm blood flow (FBF) was evaluated in response to acetylcholine, nitro-monomethyl-L-arginine (L-NMMA), and sodium nitroprusside (SNP) in subgroups of 9 controls and 7 patients with SCD. Acetylcholine induced a significantly greater FBF increase in the patients (9.7 +/- 2.9 mL/min/100 mL of forearm volume vs 2.5 +/- 1.5 mL/min/100 mL in the controls, P <.001), whereas responses to L-NMMA and SNP were similar. These results suggest that endothelial dysfunction may prevent the arterial diameter of patients with SCD from adapting to chronic or acute shear stress elevations. This may contribute to the pathophysiology of vaso-occlusive crisis in patients with SCD.
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            Author and article information

            Affiliations
            [1 ]Cardiovascular and Pulmonary Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
            [2 ]Hematology Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
            [3 ]Flow Cytometry Core Facility, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
            [4 ]Section of Pulmonary, Critical Care Medicine, Sleep and Allergy, University of Illinois, Chicago, Illinois, USA E-mail: gkato@ 123456mail.nih.gov
            Journal
            Pulm Circ
            Pulm Circ
            PC
            Pulmonary Circulation
            Medknow Publications & Media Pvt Ltd (India )
            2045-8932
            2045-8940
            Apr-Jun 2013
            : 3
            : 2
            : 448-449
            24015351 3757846 PC-3-448 10.4103/2045-8932.114784
            Copyright: © Pulmonary Circulation

            This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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            Respiratory medicine

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