CHANGES IN CELL-TO-CELL ELECTRICAL COUPLING ASSOCIATED WITH LEFT-VENTRICULAR HYPERTROPHY

Citation
M. Cooklin et al., CHANGES IN CELL-TO-CELL ELECTRICAL COUPLING ASSOCIATED WITH LEFT-VENTRICULAR HYPERTROPHY, Circulation research, 80(6), 1997, pp. 765-771
Citations number
32
Categorie Soggetti
Hematology,"Peripheal Vascular Diseas
Journal title
ISSN journal
00097330
Volume
80
Issue
6
Year of publication
1997
Pages
765 - 771
Database
ISI
SICI code
0009-7330(1997)80:6<765:CICECA>2.0.ZU;2-L
Abstract
The impedance to current flow in the intracellular compartment of guin ea pig left ventricular myocardium was measured at 20 degrees C and 37 degrees C using tissue from hypertrophied hearts subjected to aortic constriction. Alternating current of varying frequency was passed long itudinally along myocardial preparations, which revealed two time cons tants: one attributed to the surface membrane at the ends of the prepa ration and a second lying in the intracellular pathway. The longitudin al impedance was quantitatively analyzed in terms of a parallel intrac ellular and extracellular pathway; the former had two series component s, one attributable to the sarcoplasm and the other to the low-resista nce junctions between adjacent cells. This interpretation was consiste nt (1) with central experiments using n-heptanol, which increased the component attributed to intercellular junctions but not sarcoplasmic r esistivity, and (2) with suspensions of isolated myocytes, which yield ed a similar value for the sarcoplasmic resistivity. Aortic constricti on increased the heart weight-to-body weight ratio of experimental ani mals from a mean value of 3.10+/-0.28 to 5.05+/-0.83 g/kg after 50 day s 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 const riction was associated with an increased intracellular resistivity, wh ich could be attributed solely to an increase of the junctional resist ance between adjacent cells by approximate to 44% at 20 degrees C and 140% at 37 degrees 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.