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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Jan 1 1985|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)