Myocardial PO2 does not limit aerobic metabolism in the postischemic heart

Reperfused hypertrophic hearts are prone to develop reflow abnormalities, which are likely to impair O-2 return to the myocardium. Yet, reflow deficit may not be the only factor determining postischemic oxygenation in the hypertrophic heart. Altered O-2 demand may also contribute to hypoxia. In addition, the extent to which myocardial PO2 dictates energy and functional recovery in the reperfused heart remains uncertain. In the present study, moderately hypertrophied hearts from spontaneously hypertensive rats were subjected to ischemia-reperfusion, and the recovery time courses of pH and high-energy phosphates were followed by P-31 NMR. H-1 NMR measurement of intracellular myoglobin assessed tissue O-2 levels. The present study found that the exacerbation of hypoxia in the postischemic spontaneously hypertensive rat heart arises mostly from impaired microvascular supply of O-2. However, postischemic myocardial PO2, at least when it exceeds similar to 18% of the preischemic level, does not limit mitochondrial respiration and highenergy phosphate resynthesis. It only passively reflects changes in the O-2 supply-demand balance.