Effects of an increase in haemoglobin O2 affinity produced by BW12C on myocardial function in the erythrocyte‐perfused rabbit heart in vitro and myocardial infarct size in the dog

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Abstract
The effects of BW12C on myocardial function in the erythrocyte‐perfused rabbit heart and on myocardial infarct size in the anaesthetized dog have been evaluated. Perfusion of rabbit hearts with erythrocytes pretreated with BW12C (10−3 M‐4× 10−3 M) produced concentration‐dependent decreases in left ventricular pressure (LVP), LVP dP/dt and coronary perfusion pressure. A concomitant decrease in PO2 and an increase in lactate production by the myocardium was also observed. Perfusion of rabbit hearts with Krebs Henseleit buffer containing BW12C (10−5 − 10−4 M) caused no change in measured variables. Although BW12C (10−3 M) caused a small decrease in LVP, coronary perfusion pressure and heart rate, these changes were not significant. In anaesthetized dogs, an infusion of BW12C (total dose 50 mg kg−1, i.v.) caused small, but significant, changes in haemodynamic status. The oxygen saturation curve was shifted to the left and relative % oxygenation (P20) was shifted to the left throughout the course of the experiment. (P20, control 16.3 ± 0.4 mmHg; after BW12C 7.9 ± 1.4 mmHg). Pretreatment with BW12C (total dose 50 mg kg−1) caused no change in area at risk but significantly increased the myocardial infarct size by 410%. These studies with BW12C demonstrate that alteration in haemoglobin‐oxygen affinity can induce adaptive physiological changes in tissue function and metabolism and can assume a critical role when oxygen supply may be impaired due to a flow‐limiting stenosis.

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