AJP - Heart and Circulatory Physiology, Vol 243, Issue 6 917-H926, Copyright © 1982 by American Physiological Society
Passive electrical properties of normal and hypertrophied rat myocardium
E. C. Keung, C. S. Keung and R. S. Aronson
We determined the electrical constants of epicardial and endocardial
preparations from both normal and hypertrophied rat hearts. This was done
by comparative analysis of the spatial decay of steady-state electronic
voltage deflection produced by injection of a hyperpolarizing
constant-current pulse. We used a two-dimensional finite disk model to
obtain the apparent membrane resistance, (Rm)app, and internal longitudinal
resistivity (Ri), (Rm)app was significantly larger in epicardial (565 +/-
222 omega . cm2) than endocardial (375 +/- 137) preparations from normal
hearts. This regional difference disappeared in hypertrophied hearts
(epicardium 421 +/- 138, endocardium 383 +/- 121 omega . cm2). Ri was
similar for normal endocardial (272 +/- 169 omega . cm) and epicardial (326
+/- 152) preparations, as well as for hypertrophied endocardial (251 +/-
108) and epicardial (312 +/- 59) preparations. We determined the effective
membrane capacity (Ceff) by measuring the ratio of applied charge to the
displacement of membrane potential. Ceff was larger for normal hearts
(epicardium 9.7 +/- 2.5 micro F/cm2, endocardium 7.5 +/- 3.0) than for
hypertrophied hearts (epicardium 4.1 +/- 1.4, endocardium 4.7 +/- 1.2).
From the values for Ceff we calculated the effective membrane resistance,
(Rm)eff. (Rm)eff was larger for normal (epicardium 5,392 +/- 2,613 omega .
cm2, endocardium 3,013 +/- 2,096) than for hypertrophied (epicardium 1,552
+/- 633, endocardium 1,838 +/- 826) preparations. Our results show that the
amount of electrically effective membrane area is decreased in
hypertrophied myocardium, despite the increased total area per
hypertrophied cell. One functional implication of this finding is that
activation of contraction by spread of surface electrical depolarization
into the T-tubules may be impaired in hypertrophied cardiac muscle.
