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Sickle cell microvascular paradox—oxygen supply‐demand mismatch
Author(s) -
Detterich Jon A.,
Kato Roberta,
Bush Adam,
Chalacheva Patjanaporn,
Ponce Derek,
De Zoysa Madushka,
Shah Payal,
Khoo Michael C.,
Meiselman Herbert J.,
Coates Thomas D.,
Wood John C.
Publication year - 2019
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.25476
Subject(s) - medicine , perfusion , cardiology , laser doppler velocimetry , cuff , hypoxia (environmental) , oxygen saturation , ischemia , reactive hyperemia , anesthesia , blood flow , oxygen , surgery , chemistry , organic chemistry
We have previously demonstrated that sickle cell disease (SCD) patients maintain normal global systemic and cerebral oxygen delivery by increasing cardiac output. However, ischemic end‐organ injury remains common suggesting that tissue oxygen delivery may be impaired by microvascular dysregulation or damage. To test this hypothesis, we performed fingertip laser Doppler flowmetry measurements at the base of the nailbed and regional oxygen saturation (rSO 2 ) on the dorsal surface of the same hand. This was done during flow mediated dilation (FMD) studies in 26 chronically transfused SCD, 75 non‐transfused SCD, and 18 control subjects. Chronically transfused SCD patients were studied prior to and following a single transfusion and there was no acute change in rSO 2 or perfusion. Laser Doppler estimates of resting perfusion were 76% higher in non‐transfused and 110% higher in transfused SCD patients, compared to control subjects. In contrast, rSO 2 was 12 saturation points lower in non‐transfused SCD patients, but normal in the transfused SCD patients. During cuff occlusion, rSO 2 declined at the same rate in all subjects suggesting similar intrinsic oxygen consumption rates. Upon cuff release, laser doppler post occlusive hyperemia was blunted in SCD patients in proportion to their resting perfusion values. Transfusion therapy did not improve the hyperemia response. FMD was impaired in SCD subjects but partially ameliorated in transfused SCD subjects. Taken together, non‐transfused SCD subjects demonstrate impaired conduit artery FMD, impaired microcirculatory post‐occlusive hyperemia, and resting hypoxia in the hand despite compensated oxygen delivery, suggesting impaired oxygen supply‐demand matching. Transfusion improves FMD and oxygen supply‐demand matching but not microcirculation hyperemic response.