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Blood, 15 October 2009, Vol. 114, No. 16, pp. 3473-3478. Prepublished online as a Blood First Edition Paper on August 21, 2009; DOI 10.1182/blood-2009-05-223859. This Article Full Text Full Text (PDF) Supplemental Appendix and Figure All Versions of this Article: blood-2009-05-223859v1 114/16/3473    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Google Scholar Articles by Nur, E. Articles by van Lieshout, J. J. PubMed PubMed Citation Articles by Nur, E. Articles by van Lieshout, J. J. Related Collections Free Research Articles Red Cells, Iron, and Erythropoiesis Vascular Biology Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS, IRON, AND ERYTHROPOIESIS Cerebrovascular reserve capacity is impaired in patients with sickle cell disease Erfan Nur*,13, Yu-Sok Kim*,4,5, Jasper Truijen4,5, Eduard J. van Beers13, Shyrin C. A. T. Davis4,5, Dees P. Brandjes1,3, Bart J. Biemond2,3, and Johannes J. van Lieshout4,5 1 Department of Internal Medicine, Slotervaart Hospital, Amsterdam; 2 Department of Hematology, Academic Medical Centre, Amsterdam; 3 CURAMA Study Group; and 4 Department of Internal Medicine and 5 Laboratory for Clinical Cardiovascular Physiology, Centre for Heart Failure Research, Academic Medical Centre, Amsterdam, The Netherlands Sickle cell disease (SCD) is associated with a high incidence of ischemic stroke. SCD is characterized by hemolytic anemia, resulting in reduced nitric oxide-bioavailability, and by impaired cerebrovascular hemodynamics. Cerebrovascular CO2 responsiveness is nitric oxide dependent and has been related to an increased stroke risk in microvascular diseases. We questioned whether cerebrovascular CO2 responsiveness is impaired in SCD and related to hemolytic anemia. Transcranial Doppler-determined mean cerebral blood flow velocity (Vmean), near-infrared spectroscopy-determined cerebral oxygenation, and end-tidal CO2 tension were monitored during normocapnia and hypercapnia in 23 patients and 16 control subjects. Cerebrovascular CO2 responsiveness was quantified as % Vmean and µmol/L cerebral oxyhemoglobin, deoxyhemoglobin, and total hemoglobin per mm Hg change in end-tidal CO2 tension. Both ways of measurements revealed lower cerebrovascular CO2 responsiveness in SCD patients versus controls (Vmean, 3.7, 3.1-4.7 vs 5.9, 4.6-6.7 % Vmean per mm Hg, P < .001; oxyhemoglobin, 0.36, 0.14-0.82 vs 0.78, 0.61-1.22 µmol/L per mm Hg, P = .025; deoxyhemoglobin, 0.35, 0.14-0.67 vs 0.58, 0.41-0.86 µmol/L per mm Hg, P = .033; total-hemoglobin, 0.13, 0.02-0.18 vs 0.23, 0.13-0.38 µmol/L per mm Hg, P = .038). Cerebrovascular CO2 responsiveness was not related to markers of hemolytic anemia. In SCD patients, impaired cerebrovascular CO2 responsiveness reflects reduced cerebrovascular reserve capacity, which may play a role in pathophysiology of stroke. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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