Circulation, Vol 74, 1137-1146, Copyright © 1986 by American Heart Association
RL Wilensky, J Tranum-Jensen, R Coronel, AA Wilde, JW Fiolet and MJ Janse
Isolated preparations of rabbit interventricular septum were perfused
through the coronary arteries with oxygenated Tyrode's solution and placed
in a tissue bath where they were superfused as well. Transmembrane
potentials were simultaneously recorded from the subendocardium with two
flexibly mounted microelectrodes, one from a superficial cell, and the
other from a deep cell. Ischemia was produced by stopping coronary flow
while superfusion with oxygenated Tyrode's solution was maintained. After a
7 to 12 min ischemic period, the preparation was fixed by coronary
perfusion with fixative while the microelectrodes remained in place. After
fixation, the microelectrodes were withdrawn. Appropriate tissue blocks
were cut in 4 micron serial sections and the microelectrode track was
followed until the tip position was identified. Transmembrane potentials
during ischemia were divided into two categories: "border zone" potentials
(resting membrane potential [RMP] 73 +/- 3 mVe, action potential amplitude
[APA] 81 +/- 13 mV, action potential duration [APD] 116 +/- 48 msec, n =
12) and "ischemic" potentials (RMP 53 +/- 4 mV, APA 44 +/- 11 mV, APD 102
+/- 42 msec, n = 8). Ischemic potentials were recorded from cells at depths
greater than 560 micron below the endocardial surface and border zone
potentials were recorded in a layer at between 130 and 650 micron below the
surface. In a separate series of experiments, extracellular concentrations
of K+ and pH were measured with ion-sensitive electrodes at different
depths and, after a 10 min period of ischemia, part of the septum was
placed in liquid nitrogen to allow determination of phosphocreatine (PC)
levels in successive 50 to 100 micron layers. After 10 min of ischemia,
extracellular K+ gradually increased from 4 to 9 mM in endocardium to a
depth of 600 micron, pH fell from 7.4 to 6.6 over the same distance, and PC
decreased to very low, stable levels at only 800 micron. It is concluded
that in the first 10 min of acute ischemia, an endocardial border zone
exists of 40 to 60 cell layers in which transmembrane potentials are
affected relatively little by ischemia. Within this electrophysiologic
border zone extracellular K+ was lower than 9 mM, pH was higher than 6.6,
and tissue content of PC was not lower than 40% of normal. In layers deeper
than 600 micron, with further development of a metabolic gradient, action
potentials became markedly depressed. This electrophysiologic inhomogeneity
within the ischemic subendocardium could be a factor in arrhythmogenesis
during the first minutes of ischemia.
ARTICLES
The subendocardial border zone during acute ischemia of the rabbit heart: an electrophysiologic, metabolic, and morphologic correlative study
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