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Blood, 15 November 2001, Vol. 98, No. 10, pp. 3128-3131
RED CELLS
Ameliorating effects of fluorocarbon emulsion on sickle red blood
cell-induced obstruction in an ex vivo vasculature
Dhananjay K. Kaul,
Xiao-du Liu, and
Ronald L. Nagel
From the Department of Medicine, Albert Einstein
College of Medicine, Bronx, NY.
In sickle cell (SS) vaso-occlusion, the culminating event is
blockage of blood vessels by sickled red blood cells (SS RBCs). As
shown in animal models, SS RBC-induced vaso-occlusion is often partial,
allowing for a residual flow, hence oxygen delivery to partially
occluded vessels could reduce vaso-occlusion. The efficacy of an
oxygenated perflubron-based fluorocarbon emulsion (PFE) was tested for
its anti-vaso-occlusive effects in the ex vivo mesocecum vasculature
of the rat. Microvascular obstruction was induced by the infusion of
deoxygenated SS RBCs into ex vivo preparations with or without
pretreatment with platelet-activating factor (PAF). PAF induced
enhanced SS RBC-endothelium interactions, leading to greater
vaso-occlusion. Microvascular blockage resulted in increased
peripheral resistance units (PRU). Deoxygenated SS RBCs caused a
persistent 1.5-fold PRU increase in untreated preparations and
approximately a 2-fold PRU increase in PAF-treated preparations. The
greater PRU in PAF-treated preparations was caused by widespread adhesion and postcapillary blockage. Oxygenated PFE, but not
deoxygenated PFE, resulted in PRU decreases to baseline values in both
groups of experiments (with or without PAF). The PRU decrease caused by
oxygenated PFE infusion was caused by unsickling of SS RBCs in
partially occluded vessels, with no antiadhesive effect on already
adherent SS RBCs as assessed by intravital microscopy. PFE had no
effect on vascular tone. The efficacy of PFE appears to result from its
greater capacity to dissolve oxygen (10-fold higher than plasma). The
dislodgement of trapped SS RBCs and an increase in wall shear rates
will help reverse the partial obstruction. Thus, oxygenated PFE is
capable of reducing SS RBC-induced vaso-occlusion, and further
development of this approach is advisable.
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