Abstract
Nitric oxide (NO) is not only a potent gaseous vasodilator regulating blood flow, but also a reversible inhibitor of mitochondrial 02 consumption. Mathematical models for NO biotransport were recently reviewed by Buerk, who pointed out that previous models for 02 transport to tissue must be revised to include multiple effects of NO. To address this issue, we developed and solved coupled mass transport models including O2-dependent properties of NO synthases, Michaelis-Menten kinetics, and known inhibitory effects of NO on mitochondrial 02 consumption, recently reviewed by Brown.
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