Arterialization of venous blood for differentiation of sickle cell subjects in vaso-occlusive crisis

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These studies were designed as two experiments. Experiment 1 was performed to validate the hypothesis that oxygen saturation of the venous blood may be a marker for vaso-occlusive crisis (VOC) in sickle cell patients undergoing hydroxyurea (HU) treatments. Experiment 2 was performed to test the hypothesis that an acute increase in the blood nitric oxide (NO) concentration by administering HU modulates the perception of pain in sickle cell subjects in VOC. The percent saturations of oxyhemoglobin (%O 2Hb), reduced hemoblogin (%RHb), carboxy-hemoglobin (%COHb), met-hemoglobin (%MHb), fetal hemoglobin (HbF), and nitric oxide metabolites were measured in venous blood samples collected from sickle cell disease (SCD) who were on and off HU and O 2 at steady state and during VOC. The results showed the ratio of %O 2Hb/RHb in VOC + HU was significantly higher than patients in the steady state who were on and off of HU (p < 0.05). The %COHb was higher in all SCD groups, %COHb values were significantly different in SCD at steady state who were on HU. HU and O 2 treatment did not play important role on venous blood %O 2Hb and pain scores in SCD during VOC. A single oral dose of HU was associated with a significant increase in the venous concentration of nitric oxide metabolites (NOx), p < 0.05. These findings suggest that the ratio %O 2Hb/RHb in venous blood and pain scores differentiate HU-untreated and HU-treated at steady state subjects from HU-treated subjects in VOC; however, the acute increase in venous NOx produced by administering HU to HU-treated subjects in VOC does not explain this difference.

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