A. Glabe et al., CARBON-MONOXIDE INHIBITION OF REGULATORY PATHWAYS IN MYOCARDIUM, American journal of physiology. Heart and circulatory physiology, 43(6), 1998, pp. 2143-2151
The 1H nuclear magnetic resonance (NMR) myoglobin (Mb) Val Ell signal
provides a unique opportunity to assess the functional role of Mb in t
he cell. On CO infusion in perfused myocardium, the MbO(2) signal at -
2.76 parts per million (ppm) gradually disappears, whereas the corresp
onding MbCO signal emerges at -2.26 ppm, reflecting the state of Mb in
hibition. Up to 76.8% MbCO saturation, myocardial O-2 consumption (M(V
) over doto(2)) remains constant, whereas the rate-pressure product (R
PP) has already dropped to 92% of the control level. At 87.6% MbCO sat
uration, the lactate formation rate has increased by a factor of two,
and MVo(2) begins to decline. However, the ratio CO/O-2 is still 1/10,
well below the inhibition threshold for cytochrome oxidase activity.
The MVo(2) decline in the face of an adequate O-2 supply and an unpert
urbed high-energy phosphate level implies that Mb may play a role in d
irectly regulating respiration, mediated potentially by a shift in NAD
H/NAD. Although nitrite inhibits Mb, nitrite also directly affects the
myocardial function.