Myoglobin and myocardial nitric oxide

PERALTA J; LISDERO C; SCHÖPFER F; RIOBÓ N; CARRERAS MC; PODEROSO JJ

San Francisco, EEUU

Congreso; The 4th Annual Meeting of The Oxygen Society, Oxygen 97; 1997

We reported that 0.05-0.1 µM nitric oxide (•NO) decreases rat heart mitochondrial O2 uptake. Since endothelial •NO release may suggest a higher •NO cell concentration, the aim of this study was to test myocardial Mb as a regulator of •NO concentrations. Isolated and perfused rat hearts were infused 10 min with 2.5-10 µM •NO solutions. The hearts were immediately placed in liquid N2 and Mb spectra were recorded at 550-600 nm in 5-7 µm left ventricle slices. In addition, O2 uptake of perfused heart homogenates was determined with 8 mM succinate and related to additional •NO supplementation. The results showed that increasing •NO in the cardiac perfusate decreases slices oxyMb concentration from 212±12 to 115±13 µM, p<0.0001. O2 uptake and •NO detection correlated inversely with the amount of added homogenate as a function of oxyMb content, r=0.995, p<0.05. In these experiments, •NO supplementation to completely inhibit O2 uptake was lower in samples of previously •NO infused hearts. It is likely that Mb controls •NO myocardial steady-state levels in a physiological non-toxic range by binding the radical to the heme groups.