In normal hearts, myocardial perfusion is fairly well matched to regional metabolic demand, although both are distributed heterogeneously. Nonuniform regional metabolic vulnerability during
coronary stenosis would help to explain nonuniform
necrosis during
myocardial infarction. In the present study, we investigated whether metabolism-perfusion correlation diminishes during
coronary stenosis, indicating increasing mismatch of regional
oxygen supply to demand. Thirty anesthetized male pigs were studied: controls without
coronary stenosis (n = 11); group I, left anterior descending (LAD)
coronary stenosis leading to coronary perfusion pressure reduction to 70 mmHg (n = 6); group II,
stenosis with perfusion pressure of about 35 mmHg (n = 6); and group III,
stenosis with perfusion pressure of 45 mmHg combined with
adenosine infusion (n = 7). [2-(13)C]- and [1,2-(13)C]
acetate infusion was used to calculate regional O2 consumption from
glutamate NMR spectra measured for multiple tissue samples of about 100 mg dry mass in the LAD region. Blood flow was measured with
microspheres in the same regions. In control hearts without
stenosis, regional
oxygen extraction did not correlate with basal blood flow. Average myocardial O2 delivery and consumption decreased during
coronary stenosis, but vasodilation with
adenosine counteracted this. Regional
oxygen extraction was on average decreased during
stenosis, suggesting adaptation of metabolism to lower
oxygen supply after half an hour of
ischemia. Whereas regional O2 delivery correlated with O2 consumption in controls, this relation was progressively lost with graded coronary
hypotension but partially reestablished by
adenosine infusion. Therefore,
coronary stenosis leads to heterogeneous metabolic stress indicated by decreasing regional O2 supply to demand matching in myocardium during partial coronary obstruction.