The Effect of Heparin on Oxygen Transport from Blood to Tissues

Abstract

Ballistocardiographic improvement was observed after heparin administration to patients with coronary atherosclerosis in 1952. It was suggested that improved myocardial oxygenation resulted from the disappearance of chylomicrons and the larger low-density lipoproteins from the blood after the injection of heparin (1). This suggestion was verified by studies of forearm arteriovenous oxygen differences (3) and total oxygen consumption (2) in atherosclerotic patients. Tissue oxygen consumption was reduced in approximately 50% of subjects who were known to have coronary atherosclerotic disease but who were not in heart failure. After the injection of heparin, there was an average increase in oxygen consumption of 32%, whereas no increase occurred in the same subjects after injection of saline or administration of oral anticoagulants. The increase oxygen extraction occurred about 1–2 hr after intravenous injection of heparin and coincided with the time of maximal lipid clearance. These initial observations of a relation between plasma lipids, tissue oxygen consumption, and the effect of heparin have been confirmed in animals and man using various techniques (7–12, 15).