© 1997 American Heart Association, Inc.
Articles |
Changes in Cell-to-Cell Electrical Coupling Associated With Left Ventricular Hypertrophy
From the Institute of Urology and Nephrology (W.R.J.W., C.H.F.), University College London, and Academic Cardiology Unit (M.C., D.J.S.), St. Mary's Hospital Medical School, London, UK.
Correspondence to C.H. Fry, Institute of Urology and Nephrology, 67 Riding House St, London W1P 7PN, UK. E-mail chris.fry{at}ucl.ac.uk
Abstract The impedance to current flow in the intracellular
compartment of guinea pig left ventricular
myocardium was measured at 20°C and 37°C using tissue
from hypertrophied hearts subjected to aortic constriction. Alternating
current of varying frequency was passed longitudinally along myocardial
preparations, which revealed two time constants: one attributed to the
surface membrane at the ends of the preparation and a second lying in
the intracellular pathway. The longitudinal impedance was
quantitatively analyzed in terms of a parallel intracellular
and extracellular pathway; the former had two series components, one
attributable to the sarcoplasm and the other to the low-resistance
junctions between adjacent cells. This interpretation was
consistent (1) with control experiments using
n-heptanol, which increased the component attributed to
intercellular junctions but not sarcoplasmic resistivity, and (2) with
suspensions of isolated myocytes, which yielded a similar value for the
sarcoplasmic resistivity. Aortic constriction increased the heart
weight–to–body weight ratio of experimental animals from a mean value
of 3.10±0.28 to 5.05±0.83 g/kg after 50 days of constriction and
5.60±0.95 g/kg after 150 days of constriction. An increase of heart
weight–to–body weight ratio at 150 days of constriction was
associated with an increased intracellular resistivity, which could be
attributed solely to an increase of the junctional resistance between
adjacent cells by 
44% at 20°C and 140% at 37°C; the
sarcoplasmic resistivity was unchanged. The results are discussed in
terms of altered conduction in hypertrophied myocardium as
a possible basis for arrhythmias in this tissue.
Key Words: hypertrophy • longitudinal impedance • intracellular resistance