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Blood. 2014 May 15;123(20):3101-4. doi: 10.1182/blood-2013-11-533406. Epub 2014 Mar 24.

Microvascular oxygen consumption during sickle cell pain crisis.

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Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, Rockville, MD;
Infrared Imaging and Thermometry Unit, National Institute of Biomedical Imaging and Bioengineering, Bethesda, MD; and.
Hematology Branch, National Heart, Lung and Blood Institute, Bethesda, MD.


Sickle cell disease is an inherited blood disorder characterized by chronic hemolytic anemia and episodic vaso-occlusive pain crises. Vaso-occlusion occurs when deoxygenated hemoglobin S polymerizes and erythrocytes sickle and adhere in the microvasculature, a process dependent on the concentration of hemoglobin S and the rate of deoxygenation, among other factors. We measured oxygen consumption in the thenar eminence during brachial artery occlusion in sickle cell patients and healthy individuals. Microvascular oxygen consumption was greater in sickle cell patients than in healthy individuals (median [interquartile range]; sickle cell: 0.91 [0.75-1.07] vs healthy: 0.75 [0.62-0.94] -ΔHbO2/min, P < .05) and was elevated further during acute pain crisis (crisis: 1.10 [0.78-1.30] vs recovered: 0.88 [0.76-1.03] -ΔHbO2/min, P < .05). Increased microvascular oxygen consumption during pain crisis could affect the local oxygen saturation of hemoglobin when oxygen delivery is limiting. Identifying the mechanisms of elevated oxygen consumption during pain crisis might lead to the development of new therapeutic interventions. This trial was registered at as #NCT01568710.

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