Oxygen reperfusion is limited in the postischemic hypertrophic myocardium

Studies have shown that hypertrophied hearts are unusually vulnerable to ischemia. Compromised O-2 supply has been postulated as a possible explanation for this phenomenon on the basis of elongated O-2 diffusion distance and altered coronary vasculature found in hypertrophied myocardium. To examine the postulate, perfused heart experiments followed the metabolic and functional responses of hypertrophic myocardium to ischemia. H-1/P-31 NMR was used to measure cellular oxygenation and energy level during ischemia-reperfusion. The left ventricles from spontaneously hypertensive rats (SHR) were enlarged by 48%. With this moderate degree of hypertrophy, cellular O-2 and energy levels were normal during baseline perfusion. After an ischemic episode, however, cellular O-2 was severely deprived in the SHR hearts compared with the normal hearts. Depressed postischemic O-2 reperfusion correlated well with depressed energetic and functional recovery. The results from the current study thus demonstrate a critical relationship between reperfused O-2 level and functional recovery in hypertrophic myocardium. The role of reperfused O-2, however, is time dependent. During early reperfusion, factor(s) other than O-2 appear to limit functional recovery. It is when the mechanical function of the heart approaches a new steady state that O-2 becomes a dominant factor. Meanwhile, the finding of a normal O-2 level in preischemic SHR hearts defies the notion of preexisting hypoxia as a primer of ischemic damage.