Endothelium-dependent and endothelium-independent vasodilatation of the cutaneous circulation in sickle cell disease
Article first published online: 15 DEC 2010
© 2010 The Authors. European Journal of Clinical Investigation © 2010 Stichting European Society for Clinical Investigation Journal Foundation
European Journal of Clinical Investigation
Volume 41, Issue 5, pages 546–551, May 2011
How to Cite
Mohan, J. S., Lip, G. Y.H., Blann, A. D., Bareford, D. and Marshall, J. M. (2011), Endothelium-dependent and endothelium-independent vasodilatation of the cutaneous circulation in sickle cell disease. European Journal of Clinical Investigation, 41: 546–551. doi: 10.1111/j.1365-2362.2010.02444.x
- Issue published online: 6 APR 2011
- Article first published online: 15 DEC 2010
- Received 22 August 2010; accepted 5 November 2010
- laser doppler flowmetry;
- sickle cell disease;
- sodium nitroprusside
Eur J Clin Invest 2011; 41 (5): 546–551
Background Whilst there is evidence of endothelial dysfunction in sickle cell disease (SCD), whether this affects regulation in the microcirculation is not known.
Methods We studied 19 patients with SCD, eight with sickle cell-haemoglobin C (HbSC), 11 with homozygous sickle cell (HbSS) disease and 11 matched control subjects with normal haemoglobin genotype (HbAA). Vasodilator responses were evoked by iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP) in finger and forearm, cutaneous red cell flux (RCF) being measured by laser Doppler fluximetry.
Results Increases in RCF evoked in the finger by ACh were not different between SCD and HbAA subjects (P = 0·789), but were smaller in patients with HbSS than HbSC (P < 0·05). By contrast, increases in RCF evoked in forearm by ACh were greater in SCD than HbAA subjects (P < 0·05) and similar in patients with HbSC and HbSS. Increases in RCF evoked by SNP did not differ between patients with SCD and HbAA subjects in finger or forearm.
Conclusions Our results indicate that endothelium-dependent cutaneous vasodilatation is augmented in forearm of patients with SCD relative to HbAA subjects, but impaired in the finger of SCD patients with the more severe HbSS genotype. Thus, endothelial dysfunction associated with SCD is not accompanied by generalised impairment in endothelium-dependent dilatation, but with more localised impairment that includes the fingers of patients with HbSS.