Purkinje-muscle coupling and endocardial response to hyperkalemia, hypoxia, and acidosis

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Abstract
Previously we found that combined hyperkalemia, hypoxia, and acidosis depressed the electrical activity of canine epicardium more than that of endocardium or Purkinje fibers. In this study, we determined whether the resistance of endocardium to these components of ischemia was due to electrotonic interactions with Purkinje fibers. The effects of combined hyperkalemia, hypoxia, and acidosis were tested on endocardial cells that were electrically uncoupled from Purkinje cells ("uncoupled" endocardium), due to their location or to prior exposure to elevated [Ca2+]. During control, action potentials in uncoupled endocardium had shorter durations than endocardium coupled to Purkinje ("coupled" endocardium), but had similar amplitudes, upstroke velocities, and resting potentials. During combined hyperkalemia, hypoxia, and acidosis, action potentials in uncoupled endocardium were more depressed than in coupled endocardium and resembled those in depressed epicardium. In addition, the combination of these components of ischemia produced electrical uncoupling at the Purkinje-muscle junction, although each component alone did not. Thus the resistance of endocardial cells to some components of ischemia appears to involve electrotonic interactions with Purkinje cells, which may be prevented by ischemia-induced electrical uncoupling.