Myoglobin translational diffusion in rat myocardium and its implication on intracellular oxygen transport

Current theory of respiratory control invokes a role of myoglobin (Mb)-facilitated O-2 diffusion in regulating the intracellular O-2 flux, provided Mb diffusion can compete effectively with free O-2 diffusion. Pulsed-field gradient NMR methods have now followed gradient-dependent changes in the distinct H-1 NMR gamma CH3 Val E11 signal of MbO(2) in perfused rat myocardium to obtain the endogenous Mb translational diffusion coefficient (D-Mb) of 4.24 x 10(-7) cm(2) s(-1) at 22 degrees C. The D-Mb matches precisely the value predicted by in vivo NMR rotational diffusion measurements of Mb and shows no orientation preference. Given values in the literature for the Krogh's free O-2 diffusion coefficient (K-0), myocardial Mb concentration and a partial pressure of O-2 that half saturates Mb (P-50), the analysis yields an equipoise diffusion P-O2 of 1.77 mmHg, where Mb and free O-2 contribute equally to the O-2 flux. In the myocardium, Mb-facilitated O-2 diffusion contributes increasingly more than free O-2 diffusion when the P-O2 falls below 1.77 mmHg. In skeletal muscle, the P-O2 must fall below 5.72 mmHg. Altering the Mb P-50 induces modest change. Mb-facilitated diffusion has a higher poise in skeletal muscle than in myocardium. Because the basal P-O2 hovers around 10 mmHg, Mb does not have a predominant role in facilitating O-2 transport in myocardium but contributes significantly only when cellular oxygen falls below the equipoise diffusion P-O2.