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Am J Physiol Heart Circ Physiol 274: H2143-H2151, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 6, H2143-H2151, June 1998

Carbon monoxide inhibition of regulatory pathways in myocardium

Alan Glabe, Youngran Chung, Dejun Xu, and Thomas Jue

Department of Biological Chemistry, University of California, Davis, California 95616-8635

The 1H nuclear magnetic resonance (NMR) myoglobin (Mb) Val E11 signal provides a unique opportunity to assess the functional role of Mb in the cell. On CO infusion in perfused myocardium, the MbO2 signal at -2.76 parts per million (ppm) gradually disappears, whereas the corresponding MbCO signal emerges at -2.26 ppm, reflecting the state of Mb inhibition. Up to 76.8% MbCO saturation, myocardial O2 consumption (MVO2) remains constant, whereas the rate-pressure product (RPP) has already dropped to 92% of the control level. At 87.6% MbCO saturation, the lactate formation rate has increased by a factor of two, and MVO2 begins to decline. However, the ratio CO/O2 is still 1/10, well below the inhibition threshold for cytochrome oxidase activity. The MVO2 decline in the face of an adequate O2 supply and an unperturbed high-energy phosphate level implies that Mb may play a role in directly regulating respiration, mediated potentially by a shift in NADH/NAD. Although nitrite inhibits Mb, nitrite also directly affects the myocardial function.

myoglobin; nuclear magnetic resonance; respiration; oxidative phosphorylation


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