The role of myoglobin in retarding oxygen depletion in anoxic heart.

The present study explores the role of myoglobin (Mb) in retarding the development of anoxia in the perfused working rat heart. We examine this phenomenon by analyzing the behavior and the kinetics of Mb oxygenation and cytochrome aa3 (cytaa3) redoxation. Absorbance changes, measured at wavelength pairs specific to Mb and cytaa3, show parallelism between the Mb oxygenation status and the redox states of cytaa3. Induction of anoxia leads to early and accelerated Mb deoxygenation whereas cytaa3 reduction marks a slight delay and its rate is twice slower than that of Mb. Then, when Mb is desatured above 50%, the cytaa3 reduction becomes accelerated. With the reoxygenated perfusion following the anoxia, the rate of Mb reoxygenation is twice faster than that of the cytaa3 reoxidation. When the oxygen-binding function of Mb, in situ in the heart, is abolished by treatment with sodium nitrite (NaNO2), the redox kinetics of cytaa3 show significant perturbations. Induction of anoxia leads to a precocious and accelerated reduction of cytaa3, compared to the same anoxic heart before the treatment. At reoxygenation, the reoxidation rate of cytaa3 decreases significantly, compared to that before the treatment. Similarly, in the nitrite treated heart, the phosphocreatine (PCr) level decreases to 60% of the control, whereas the inorganic phosphate (Pi) level increases to 300%. ATP concentration, however, remains constant. We conclude from these results that Mb may support mitochondrial respiration at the critical levels of the myocardial O2 supply.