Acute Change in Hemoglobin Affinity for Oxygen during Angina Pectoris

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Abstract
The hypothesis that a decrease in hemoglobin affinity for oxygen is a compensory mechanism to increase oxygen delivery to ischemic myocardium was tested in six patients with angina pectoris. Blood was drawn simultaneously from radial artery and coronary sinus. Oxygen tension at 50 per cent saturation (P50) and erythrocytic 2,3-diphosphoglycerate, adenosine triphosphate and pH measured before, during and after angina pectoris produced by atrial pacing showed no significant difference at rest. The longer the duration of angina pectoris, the more coronary-sinus P50 exceeded arterial P50. After four to 10 minutes of angina, the difference was 0.6 to 2.9 mm of mercury. One patient, in whom ST-segment depression and lactate production but no angina pectoris developed, had no change in hemoglobin affinity for oxygen. Decreased hemoglobin affinity for oxygen was not accompanied by change in erythrocytic 2,3-diphosphoglycerate, adenosine triphosphate and pH. The rapid decrease in affinity enhances myocardial oxygen delivery during angina pectoris.