Incomplete coronary vasodilation during myocardial ischemia in swine

To determine if endogenous (ENDG) vasodilation was maximum during myocardial ischemia, left anterior descending (LAD) mean pressure (P) was reduced for 20 min in 13 swine. At LAD P of 45 mmHg (LAD P45) flow fell during ENDG = 25 but rose to 44 ml/min during adenosine (AD) infusion (P < 0.01). Flow increased to subendocardium (ENDG 0.65 vs. AD 1.04 ml·min^-1·g^-1) and to subepicardium (ENDG 0.99 vs. AD 1.83 ml·min^-1·g^-1; P < 0.05). No significant change occurred in myocardial O₂ consumption (MV̇O₂; ENDG 2.91 vs AD 3.18 ml·min^-1·g^-1), lactate extraction (ENDG = -5 vs AD -1%), and wall thickening (WTh; ENDG +16 vs. AD +17%). At LAD P35, flow during ENDG was 12 but rose to 19 ml/min during AD (P < 0.01). Flow increased to subendocardium (ENDG 0.24 vs. AD 0.46 ml·min^-1·g^-1; P < 0.02) and subepicardium (ENDG 0.51 vs. AD 0.87 ml·min^-1·g^-1; P < 0.01). No significant change occurred in MV̇O₂ (ENDG 1.38 vs. AD 1.59 ml/min), lactate extraction (ENDG -38 vs. AD -22%), WTh (ENDG -1 vs. AD +1%). Thus endogenous vasodilation reserve was not used fully during ischemia. AD increased flow but did not improve abnormalities in myocardial function or metabolism.