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Laser Scanner Observations of Heterogeneous Conduction Patterns in Rabbit Epicardium Induced by Cellular Uncoupling with Heptanol
Author(s) -
HILL BRUCE C.,
COURTNEY KENNETH R.,
DELMAR MARIO
Publication year - 1990
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1990.tb01075.x
Subject(s) - thermal conduction , heptanol , coupling (piping) , biophysics , anatomy , electrophysiology , gap junction , biomedical engineering , materials science , chemistry , medicine , intracellular , biology , biochemistry , metallurgy , composite material
Heptanol Disrupts Epicardial Conduction . This study examines how severely reduced intercellular electrical coupling affects the pattern of activation of left ventricular rahhit epicardium. Five thin (< 1‐mm thick) flaps of < 60 mm 2 were stained in vitro with potentiometric dye WW781. A helium‐neon laser beam was scanned over 63 spots on each flap, and the voltage‐dependent fluorescence intensity from each spot was used to construct maps of the activation resulting from pacing at a single site. Introducing heptanol (1.75 mM) produced lines of conduction hlock in four of the five preparations after times ranging from 7 to 71 minutes; at varying intervals during this time, activation patterns were obtained. Fiber orientation was later determined from histologic sections. Heptanol changed the relatively uniform conduction seen under control conditions to heterogeneous patterns having regions of slowed conduction and lines of partial and complete block oriented predominantly parallel to the fiber direction (i.e., transverse propagation was blocked). The two partial blocks, which did not extend across the entire tissue, caused the activation wave to pivot around one end of the block line. The subsequent retrograde activation of the line's distal side was consequently delayed. Two points on opposite sides of these hlocks, separated by < 1 mm, had activation times differing by as much as 89 msec rather than a normal 3–5 msec. Thus, sufficient uncoupling can alter conduction pathways on the scale of a few millimeters. The resulting dispersion in activation times at closely spaced points may predispose poorly‐coupled cardiac tissue to development of reentrant arrhythmias. (J Cardiovasc Electrophysiol. Voi. I, pp, 426–436. October 1990)