Effects of High Arterial Oxygen Tension on Coronary Blood Flow Regulation and Myocardial Oxygen Delivery

Abstract

The effects of high oxygen tension, or hyperoxia,on the control of myocardial blood flow are both complex and controversial. Substantial evidence suggests that high arterial oxygen tension has a direct vasoconstrictor effect (Baron et al.,1990; Bourdeau-Martini et al.,1974; Ishikawa et al.,1984; Lammerant et al.,1969; Sobol et al.,1962), similar to the vasoconstrictor effects oxgyen demonstrates in other tissues (Daugherty et al.,1967; Duling and Pittman,1975; Sullivan and Johnson,1981). It is often difficult, however, to distinguish direct vasoconstrictor effects from other, indirect effects of oxygen which also cause coronary vasoconstriction. For example, increasing arterial oxygen tension causes multiple direct and reflex hemodynamic effects, including reduced heart rate Ganz et al.,1972; Kenmure et al.,1971; Whalen et al.,1965) and decreased ventricular wall tension (Ishikawa et al.,1984; Ishikawa et al.,1982), both of which may reduce myocardial oxygen demand and which may therefore lead to coronary vasoconstriction by metabolic regulation mechanism. Additionally, higher oxygen tension is generally associated with higher oxygen content, so it might expected that when arterial oxygen tension is raised beyond the normal range (raising oxygen content slightly), that the metabolic regulation mechanisms of the heart would induce vasoconstriction, reducing blood flow slightly, but maintaining constant oxygen delivery.