Myocardial Blood Flow and Oxygen Consumption during Postprandial Lipemia and Heparin-Induced Lipolysis

Abstract

The role of the physical state of plasma as a determinant of oxygen availability to the myocardium has been investigated during the course of alimentary lipemia. After the development of substantial plasma lactescence, the coronary blood flow (nitrous oxide method) and myocardial oxygen consumption were assessed in 7 normal human subjects and repeated after heparin-induced lipolysis. The lipemic state was further contrasted with a control fasting group, comparable in age and sex. The mean coronary blood flow for 15 fasting controls was 83 ml. per 100 Gm. of left ventricle per minute with a myocardial oxygen extraction of 11.04 volumes per cent, and a myocardial oxygen consumption of 9.0 ml. per 100 Gm. of left ventricle per minute. By contrast, the mean coronary blood flow during maximal lipemia in the 7 subjects fed cream was 20 per cent below normal, with a value of 67 ml. per 100 Gm. per minute ( p =< 0.01). As the extraction of oxygen was not significantly affected, the calculated myocardial oxygen consumption was proportionately reduced to 7.02 ml. per 100 Gm. per minute ( p =< 0.01). A failure of the anticipated oxygen extraction increment in the face of coronary blood flow reduction suggests an impediment of blood-tissue oxygen transport during lipemia. After the administration of 60 mg. of heparin to the 7 lipemic subjects, a 65 per cent decline in plasma lactescence was observed by 45 minutes, when the coronary blood flow and myocardial oxygen consumption were elevated to 87 ml. per 100 Gm. per minute ( p =< 0.05) respectively. Thus, the reduced coronary flow and myocardial oxygen consumption were restored in each instance to normal levels during the process of plasma clearing. There were no associated systemic hemodynamic changes to account for such increments. These heparin effects appear dependent on the lipemia-clearing property, for no alteration in coronary dynamics was found in 6 additional patients in whom this activity was not manifest after the same heparin dosage. The residual lactescence after post-heparin lipolysis was associated with no significant deviation of coronary dynamics from the normal. That a concentration-dependent phenomenon is operative, was confirmed in a separate group of patients in whom low lactescence values developed in the course of alimentary lipemia without affecting myocardial oxygen consumption. The relevance of the lipemic state, per se, to the pathophysiology of myocardial ischemia appears to depend upon the establishment of an oxygen gradient within the myocardium, presumably through altered pressure-flow relationships produced by lipemic blood within a pathologic vessel.