An electric field mechanism for transmission of excitation between myocardial cells.

A long-standing dogma in basic electrophysiology of the heart has been that the atrial and ventricular myocardial cells are interconnected by low-resistance pathways mediated by gap-junction connexon channels.1 This dogma became established based on the publications of a number of investigators, including Weidmann,2 Woodbury and Crill,3 and DeMello.4 It was concluded that the input resistance of myocardial cells in a bundle was very low (eg, 30 KΩ), the length constant (λ) of the bundle was very long (eg, 1.5 mm), and that local-circuit action current spreads readily from cell to cell. The ultrastructure of mammalian myocardium showed presence of numerous gap junctions.5 This dogma has become ingrained in most textbooks and advanced reference books dealing with the heart. This dogma still lives on despite the facts that it is now accepted that the input resistance is high (eg, 5 to 40 MΩ) and the length constant is very short (eg, 150 to 350 μm) (see references in Sperelakis and McConnell6,7⇓). For example, an input resistance for myocardial cells, measured in isolated cell pairs, was ≈27 to 37 MΩ,8 and the λ value for myocardial bundles was reported to be 357 μm.9 Propagation in cardiac muscle is now accepted as being discontinuous (or saltatory) in nature.10 In addition, gap junctions are scarce or absent in the hearts of nonmammalian vertebrates, such as birds, lizards, frogs, and fish (for references, see Reference 6). Despite this, the hearts in those lower vertebrates function normally. The low-resistance dogma was first challenged in 1959 by Sperelakis and colleagues,11 in experiments on frog heart. Subsequently, they published a series of studies on mammalian hearts based on biophysical measurements and demonstrated that, in many cases, there were not low-resistance connections between myocardial cells. Most of this …