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Department of Biomedical Engineering and Center for Computational Medicine and Biology, School of Medicine, The Johns Hopkins University, Baltimore, Maryland 21205
Administration of
hemoglobin-based oxygen carriers (HBOCs) frequently results in
vasoconstriction that is primarily attributed to the scavenging of
endothelium-derived nitric oxide (NO) by cell-free hemoglobin. The
ensuing pressor response could be caused by the high NO reactivity of
HBOC in the vascular lumen and/or the extravasation of hemoglobin
molecules. There is a need for quantitative understanding of the NO
interaction with HBOC in the blood vessels. We developed a detailed
mathematical model of NO diffusion and reaction in the presence of an
HBOC for an arteriolar-size vessel. The HBOC reactivity with NO and
degree of extravasation was studied in the range of 2-58 × 106 M
1 · s1 and
0-100%, respectively. The model predictions showed that the addition of HBOC reduced the smooth muscle (SM) NO concentration in the
activation range (12-28 nM) for soluble guanylate cyclase, a major
determinant of SM contraction. The SM NO concentration was
significantly reduced when the extravasation of HBOC molecules was
considered. The myoglobin present in the parenchymal cells scavenges
NO, which reduces the SM NO concentration.
mathematical model; microcirculation; extravasation; vasoconstriction; myoglobin
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