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We have studied the effect of a decrease in hemoglobin-O2 affinity (increased P50) on O2 delivery in the non-paced, isolated, blood-perfused rat heart before and after coronary vasodilatation with and without an increase in myocardial O2 consumption (MVO2) produced with isoproterenol. Changes in perfusate P50 were produced with orthoiodosodium benzoate (OISB). Low concentrations of isoproterenol (0.74 micrograms/liter) caused no significant changes in coronary blood flow (QCOR) or MVO2 per beat. Perfusion with OISB-treated (8 mM) blood increased P50 from 29 to 33 mmHg at constant pH. MVO2 per beat increased significantly, QCOR did not change, and the ratio QCOR/MVO2, a reflection of the flow/metabolism distribution, decreased to values obtained in the absence of isoproterenol. With high doses of isoproterenol (5.0 micrograms/liter), MVO2 per beat and QCOR/MVO2 increased. Addition of OISB (13 mM) increased P50 from 29 to 39 mmHg, with no significant reduction in either QCOR or the QCOR/MVO2 ratio. Our data suggest that a decrease in blood-O2 affinity affects myocardial O2 delivery depending on the initial metabolic requirement: at basal MVO2 changes in the distribution of myocardial blood flow are probably secondary to the effects of PO2 on vessels that supply metabolically less active regions; at high MVO2 and following a maximum increase in capillary density, changes in vascular PO2 appear less effective than locally generated metabolic vasodilators, and distribution of blood flow is unaffected.

Dependency of O2-affinity effects on O2 consumption in the isolated rat heart.