Electrotonically mediated delayed conduction and reentry in relation to "slow responses" in mammalian ventricular conducting tissue.

A narrow zone of block in isolated false tendon preparations was created by perfusion of the central compartment (gap) of a three-compartment tissue bath with either an isotonic sucrose solution or a solution designed to mimic the extracellular milieu in ischemic tissue. Driven responses on the proximal side of the gap were transmitted to the distal side after long delays. The characteristics of the "ischemic" gap model were found to be qualitatively similar to those of the sucrose gap model in which impulse transmission is electrotonically mediated. In both models, the effects of driven action potentials were mimicked by electrotonic displacement of membrane potential by current pulses passed across the gap. Foot-potentials representative of electrotonic potentials bringing the distal membrane to threshold were present in all cases and were found to be largely unaffected by the slow channel-blocking agent, verapamil. Transmembrane activity recorded from the central portion of the gap segment was shown to be electrotonic in nature. Ectopic activity in the form of reflected reentry was readily demonstrable in the ischemic gap model in the presence or absence of verapamil as well as in the sucrose gap model. When propagation across the gap was mediated by "slow" responses, transmission was relatively prompt and reentry did not occur. Our observations suggest that very slow conduction through ischemic areas may result from step delays imposed by electrotonic transmission of impulses across inexcitable segments of cable rather than from uniform slow conduction of propagated action potentials with slow upstrokes.