The mechanism underlying heterogeneous pH in ischemic and reperfused myocardium.

The mechanism responsible for heterogeneity in tissue pH was investigated in perfused rat hearts subjected to ischemia/reperfusion insult, by correlating the time course of pH changes to the severity of vascular impairment. In 25 perfused hearts, myocardial pH was monitored by 31 P-NMR spectra. During ischemia, pH, which was 7.1 at the beginning of ischemia, progressively decreased and reached a steady level of 5.9 (5.9-compartment) after 40 minutes. In addition, another define peak of pH 7.1 (7.1-compartment) became evident after 50 min of ischemia. The 7.1-compartment grew higher with ischemic time and was only observed after 180 min of ischemia. Although reperfusion after 20 min of ischemia recovered pH, ATP, and creatine phosphate, reperfusion after 50 min left two Pi peaks, the 5.9- and 7.1-compartments; the former gradually decreased with a concomitant increase of the latter. Reperfusion after 180 min of ischemia with various pH levels did not shift the Pi peak from pH 7.1, suggesting that the perfusate did not reach that compartment, the impaired flow region. High coronary resistance and a heterogeneous staining pattern concomitant with a late appearance of the 7.1 component further supported this hypothesis. Myocardial coenzyme Q10 radical, an indicator of the tissue redox state, was also low in those hearts which were reperfused after 50 min of ischemia. Thus, the splitting of the Pi peak, caused by reperfusion after prolonged ischemia, represents the existence of a no-reflow region.