Post-ischemic "stunned" myocardium appears to be metabolically inefficient, since oxygen consumption is preserved, while mechanical work is depressed. The present study investigated whether this metabolic inefficiency represents a basal functional abnormality present in the quiescent myocardium (e.g. abnormal mitochondrial coupling) or is specifically related to muscle contraction. Isolated perfused rabbit hearts (n = 7) were exposed to 20 min zero-flow ischemia to produce post-ischemic myocardial stunning. After 10 min of reperfusion, mean rate-pressure product (mmHg/min), was reduced to 56.1% of baseline in stunned hearts, while mean oxygen consumption (μmol O2/min/g LV) was reduced to only 71.8% of baseline. The ratio of oxygen consumption to rate-pressure product remained significantly elevated throughout 40 min of reperfusion when compared with non-ischemic controls (P < 0.01). Despite inappropriately high oxygen consumption in the beating stunned heart, basal oxygen consumption measured after KCl arrest was not significantly different from controls (1.07 ± 0.07 vs. 1.03 ± 0.04, respectively). These results indicate that the metabolic inefficiency found in stunned myocardium is not a basal abnormality, but rather is related specifically to abnormalities in contraction or electromechanical coupling.
- Cardiac contraction
- Cardiac work
- Myocardial oxygen consumption
- Stunned myocardium
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine