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Blood, 15 March 2001, Vol. 97, No. 6, pp. 1584-1589
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Endothelial dysfunction in patients with sickle cell disease is
related to selective impairment of shear stress-mediated
vasodilation
Laurent Belhassen,
Gabriel Pelle,
Saïd Sediame,
Dora Bachir,
Claudine Carville,
Catherine Bucherer,
Catherine Lacombe,
Frederic Galacteros, and
Serge Adnot
From the Service de Physiologie-Explorations
Fonctionnelles and the Centre de la Drépanocytose, Hôpital
Henri Mondor, APHP et Université Paris XII, France; and
Unité de Biorhéologie, Université Paris VI et LBHP
CNRS ESA 7057, France.
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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