Microcirculatory adaptations in sickle cell anemia: reactive hyperemia response.
With the technique of laser-Doppler velocimetry, cutaneous blood flows in the forearm of patients with stable sickle cell disease after graded periods of proximal ischemia were compared with normal subjects matched for age, race, and sex, and with patients with anemia caused by beta(+)-thalassemia. In the sickle cell patients the reactive hyperemia was characterized by an increased time interval between the release of the occlusion and the peak amplitude response (time-to-peak) and by a greater period of blood flow above the base-line value (payback ratio) compared with controls. In addition, prolongation of the occlusion period led to an augmentation in the magnitude of the characteristic basal flow oscillations or an induction of this phenomenon at sites not exhibiting it before ischemia. Base-line or ischemia-provoked flow oscillations of either this magnitude or frequency were only observed in normal or thalassemic controls during brief intervals in the rapidly decaying portion of the hyperemic response and in one subject with homozygous hemoglobin C disease. These results would support a model of a local integrative control of microcirculatory blood flow, which appears to become augmented, synchronized, and sustained in sickle cell subjects.
Laboratory of Chemical Biology, National Institute of Diabetes, and Digestive and Kidney Diseases, Bethesda, Maryland 20892.
G P
GP
Rodgers
A N
AN
Schechter
C T
CT
Noguchi
H G
HG
Klein
A W
AW
Nienhuis
R F
RF
Bonner
D000222:Adaptation, Physiological; D000328:Adult; D000755:Anemia, Sickle Cell / Q000503:physiopathology* / Q000628:therapy; D001783:Blood Flow Velocity; D005078:Exchange Transfusion, Whole Blood; D005260:Female; D006453:Hemoglobinopathies / Q000503:physiopathology; D006358:Hot Temperature; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology*; D007834:Lasers; D008297:Male; D008833:Microcirculation; D010146:Pain; D014463:Ultrasonography