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Myoglobin Translational Diffusion in Myocardium and Its Implication on Intracellular Oxygen Transport.

Authors: Lin, PC  Kreutzer, U  Jue, T 
Citation: Lin PC, etal., J Physiol. 2006 Oct 12;.
Pubmed: (View Article at PubMed) PMID:17038435
DOI: Full-text: DOI:10.1113/jphysiol.2006.116061

Current theory of respiratory control invokes a role of myoglobin (Mb) facilitated O2 diffusion in regulating the intracellular O2 flux, provided Mb diffusion can compete effectively with free O2 diffusion. Pulsed-field gradient NMR methods have now followed gradient dependent changes in the distinct 1H NMR gamma CH3 Val E11 signal of MbO2 in perfused rat myocardium to secure the endogenous Mb translational diffusion coefficient (DMb) of 4.24 x 10-7 cm2/s at 22 degrees C. The DMb matches precisely the value predicted by in vivo NMR rotational diffusion measurements of Mb and shows no orientation preference. Given literature values for the Krogh's free O2 diffusion coefficient (K0), myocardium Mb concentration, and a partial pressure of O2 that half saturates Mb (P50), the analysis yields an equipoise diffusion PO2 of 1.77 mm Hg, where Mb and free O2 contribute equally to the O2 flux. In the myocardium, Mb facilitated O2 diffusion contribute increasingly more than free O2 diffusion when the PO2 falls below 1.77 mm Hg. In skeletal muscle, the PO2 must fall below 5.72 mm Hg. Altering the Mb P50 induces only a modest change. Mb facilitated diffusion has a higher poise in skeletal muscle than in myocardium. Because the basal PO2 hovers around 10 mm Hg, Mb does not have a predominant role in facilitating O2 transport but contributes significantly only when cellular oxygen falls below the equipoise diffusion PO2.


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RGD Object Information
RGD ID: 1582398
Created: 2006-11-07
Species: All species
Last Modified: 2006-11-07
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.