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Articles in PresS, published online ahead of print February 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00972.2001
Submitted on November 7, 2001
Accepted on February 12, 2002
1 Department of Biomedical Engineering and Center for Computational Medicine and Biology, The Johns Hopkins University, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: kavdia{at}bme.jhu.edu.
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 x106 M-1s-1 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.
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