We studied the time course, magnitude and homogeneity of the change in extracellular myocardial potassium activity after acute ligation of the left anterior descending coronary artery in pigs using potassium-sensitive electrodes made from a valinomycin-polyvinyl chloride matrix membrane. We also studied the relationship between the changes in potassium activity and the simultaneous changes in ventricular activation using the reference barrel of the K+ electrode to record ventricular electrograms. We found that the K+ rose sooner, more rapidly and to higher levels than previously reported. The K+ changes occurred in three phases: a phase of rapidly rising K+ that began within seconds of the ligation and lasted 5-15 minutes, a plateau phase that lasted approximately 15 minutes and a phase of slowly rising K+ that extended throughout the longest occlusion (60 minutes) used in this study. The K+ changes were reversed by release of the occlusion during the rapidly rising and plateau phases, but were not reversed by release of the occlusion during the phase of slowly rising K+. Inhomogeneities in the K+ rise appeared between the center and lateral margins of the midmyocardial ischemic zone, between the subendocardium and the subepicardium in the center of the ischemic zone, and between closely spaced electrodes located in the midmyocardial center of the ischemic zone. Thus, the change in K+ activity, as recorded by our electrodes, can be considered an excellent marker of ischemia. Changes in ventricular activation paralleled the K+ rise, the inhomogeneities of K+ rise and the reversal of the K+ rise after release but could not be entirely explained by the change in K+.
Hill et al. (Tue,) studied this question.