Resting potential changes associated with Na-K pump in failing heart muscle

Microelectrode and single sucrose gap techniques were used to measure transmembrane potentials in normal and failing papillary muscles. Six muscles from control animals and 10 from banded animals were cooled (2-4 degrees C) and subsequently rewarmed to 37 degrees C. Normal muscles demonstrated significantly greater increases in maximum diastolic potential (--Emax) on rewarming than those from failing animals. In muscles subjected to transient periods of rapid stimulation, --Emax depolarized initially on stimulation but eventually plateaued at a depolarized level and then hyperpolarized beyond prestimulation levels. These changes in --Emax were altered in failing muscles. The initial rate of depolarization (delta -- Emax/delta t) on stimulation and the magnitude of this depolarization (delta -- Emax) was decreased at all rates studied. The time necessary to arrive at the plateau (time to delta -- Emax) was significantly lengthened in failing muscles. The hyperpolarization seen on rewarming cooled preparations and the changes in --Emax during stimulation have both been related to an activation of an electrogenic Na-K pump suggesting that this ion-transport system is altered in failing heart muscle. The decrease in delta -- Emax/delta t and delta -- Emax seen in failing muscles indicates that K efflux may be lower or that the volume of confined intercellular spaces is greater in failing heart muscle.