title: Imaging hemoglobin oxygen saturation in sickle cell disease patients using noninvasive visible reflectance hyperspectral techniques: effects of nitric oxide.
abstract: Sickle cell disease is characterized by microvascular occlusion and hemolytic anemia, factors that impair tissue oxygen delivery. We use visible reflectance hyperspectral imaging to quantitate skin tissue hemoglobin oxygen saturation (HbO2) and to determine whether changes in blood flow during nitric oxide (NO) stimulation or gas administration (therapies proposed for this disease) improve skin tissue oxygen saturation in five patients with sickle cell disease. Compared with six healthy African-American subjects, sickle cell patients exhibited higher forearm blood flows (7.4 +/- 1.8 vs. 3.2 +/- 0.4 ml.min-1.100 ml tissue-1, P = 0.037) but significantly reduced percentages of skin HbO2 (61.0 +/- 0.2 vs. 77.5 +/- 0.2%, P < 0.001). Administration of acetylcholine to patients increased blood flow by 15.1 +/- 3.8 ml.min-1.100 ml tissue-1 and the percentage of skin HbO2 by 4.1 +/- 0.3% (P = 0.02, P < 0.001, respectively, from baseline values). Sodium nitroprusside, a direct NO donor, increased blood flow by 3.9 +/- 1.1 ml/min and the percentage of skin HbO2 by 2.9 +/- 0.3% (P = 0.02, P < 0.001, respectively). NO inhalation had no effect on forearm blood flow, yet increased the percentage of skin HbO2 by 2.3 +/- 0.3% (P < 0.001). Percentages of skin HbO2 were exponentially related to blood flow (R = 0.97, P < 0.001), indicating a limit to skin tissue oxygen saturation at high blood flows. Thus, for acetylcholine infusion leading to blood flows sevenfold greater than those of healthy resting African-American subjects, patients still exhibited lower percentages of skin HbO2 (65.2 +/- 0.2 vs. 77.5 +/- 0.2%, P < 0.001). Visible reflectance hyperspectral imaging demonstrates that either the stimulation or the administration of NO pharmacologically or by gas inhalation improves, but does not normalize, skin tissue oxygen saturation in patients with sickle cell disease.
authors.affiliation: Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases/NIH, 9000 Rockville Pike, Bethesda, MD 20892-0510, USA.
authors.forename: Karel J
authors.initials: KJ
authors.lastname: Zuzak
authors.forename: Mark T
authors.initials: MT
authors.lastname: Gladwin
authors.forename: Richard O
authors.initials: RO
authors.lastname: Cannon
authors.forename: Ira W
authors.initials: IW
authors.lastname: Levin
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage; D000293:Adolescent; D000328:Adult; D000755:Anemia, Sickle Cell / Q000175:diagnosis / Q000378:metabolism* / Q000503:physiopathology; D001785:Blood Gas Monitoring, Transcutaneous / Q000379:methods*; D004791:Enzyme Inhibitors / Q000008:administration & dosage; D005260:Female; D006225:Hand / Q000098:blood supply; D006451:Hemoglobin, Sickle / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism*; D010108:Oxyhemoglobins / Q000378:metabolism*; D016491:Peripheral Vascular Diseases / Q000378:metabolism; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012867:Skin / Q000098:blood supply*; D014665:Vasodilator Agents / Q000008:administration & dosage; D019323:omega-N-Methylarginine / Q000008:administration & dosage
chemical_list: D004791:Enzyme Inhibitors; D006451:Hemoglobin, Sickle; D010108:Oxyhemoglobins; D014665:Vasodilator Agents; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D000109:Acetylcholine