Circulation, Vol 61, 768-778, Copyright © 1980 by American Heart Association
JL Hill and LS Gettes
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+.
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