Abstract
The contribution of myoglobin to cardiac performance and O2 consumption was investigated using an isolated perfused buffalo sculpin (Enophrys bison) heart preparation. Dose–response studies at ambient (150 Torr)(1 Torr = 133.322 Pa) O2 tensions were conducted as a means of selecting an oxidizing agent with high activity toward myoglobin, while minimizing the possibility of toxic side effects. Treatment with 10.0 μM phenylhydroxylamine oxidized greater than 95% of intracellular myoglobin but did not affect pulse pressure, peak dP/dt, or heart rate. The functional importance of myoglobin was investigated by perfusing electrically paced hearts with 10.0 μM phenylhydroxylamine at physiological (32 Torr) O2 tensions. Inactivation of myoglobin by oxidation with phenylhydroxylamine had no effect on cardiac performance or O2 consumption.
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