Oxygen reperfusion is limited in the postischemic hypertrophic myocardium.

Studies have shown that hypertrophied hearts are unusually vulnerable to ischemia. Compromised O2 supply has been postulated as a possible explanation for this phenomenon on the basis of elongated O2 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. 1H/31P 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 O2 and energy levels were normal during baseline perfusion. After an ischemic episode, however, cellular O2 was severely deprived in the SHR hearts compared with the normal hearts. Depressed postischemic O2 reperfusion correlated well with depressed energetic and functional recovery. The results from the current study thus demonstrate a critical relationship between reperfused O2 level and functional recovery in hypertrophic myocardium. The role of reperfused O2, however, is time dependent. During early reperfusion, factor(s) other than O2 appear to limit functional recovery. It is when the mechanical function of the heart approaches a new steady state that O2 becomes a dominant factor. Meanwhile, the finding of a normal O2 level in preischemic SHR hearts defies the notion of preexisting hypoxia as a primer of ischemic damage.