“…Assuming that values of coronary venous PO 2 reflect levels of myocardial tissue PO 2 (469, 919), these findings collectively support that mechanisms to invoke metabolic coronary vasodilation are progressively activated as myocardial tissue PO 2 falls below a critical threshold value. The physiologic relevance of this relationship is also supported by the essential observations that pronounced reductions in coronary microvascular resistance are also observed in response to reductions in perfusion pressure (84, 201, 252–254, 333, 690, 853), arterial PO 2 [i.e., hypoxemia; (2,22,89,205,262,376,458,608,645,670,671,708,767, 849, 917, 940, 958)], arterial oxygen content [i.e., anemia; (59, 102, 120, 204, 206–210, 323, 372, 377, 482, 486, 509, 691, 905, 934, 935, 947, 957, 976)], and overt myocardial ischemia (27–29,33,36,97,110,189,246,497,498,730–732) (see Fig. 2).…”