2017 年 76 巻 5 号 p. 201-207
Myocardial ischemia induces an increase in extracellular K+ ([K+]e) and a decrease in extracellular pH (pHe). To clarify the role of mechanical and electrical activities in these changes, we investigated the effect of 2, 3-butanedione (BDM), a specific inhibitor of actin-myosin coupling, and pinacidil, an ATP-sensitive K+ channel opener, on [K+]e, pHe, action potential duration (APD) and regional contractility during 8 minutes of ischemia in porcine hearts. We inserted K+- and pH-sensitive electrodes and a pair of ultrasonic crystals into the mid-myocardium. We also placed a floating microelectrode in the subepicardium of the ischemic zone. The carotid artery was shunted to the LAD through a roller pump, and BDM (10 mM, n = 7) or pinacidil (50 νM, n = 8) was infused to the LAD shunt in advance of no-flow ischemia. Regional systolic shortening became dyskinetic with the BDM infusion and decreased from 20.1 ± 1.6% to 4.9 ± 1.6% with pinacidil. APD was not affected by BDM, but it decreased from 348 ± 14 ms to 206 ± 14 ms (P < 0.001) with the infusion of pinacidil prior to ischemia. Both pinacidil and BDM attenuated the rise in [K+]e, but the effect of pinacidil was greater. Both agents reduced the fall in pHe, but this effect was greater with BDM. Pinacidil-induced APD shortening was maintained during ischemia; BDM did not affect APD shortening during ischemia. The fall in pHe during ischemia appears to be related mainly to mechanical activity but the corresponding increase in [K+]e is more attributable to APD.
