Evidence for two components of sodium channel block by lidocaine in isolated cardiac myocytes

C. W. Clarkson, C. H. Follmer, R. E. Ten Eick, L. M. Hondeghem, J. Z. Yeh

Research output: Contribution to journalArticlepeer-review

73 Scopus citations


The effects of lidocaine on sodium current in cardiac myocytes isolated form cat and guinea pig were investigated using the whole-cell variation of the patch-clamp technique. Lidocaine (43-200 μM) reduced sodium current during repetive depolarizing pulses in a use-dependent manner. To clarify the nature of the use-dependent block, we characterized the time course of block development using a two-pulse protocol. Two distinct phases of block development were found: a rapid phase (τ = 1-6 msec) having a time course concurrent with the time course of channel activation, and a slower phase (τ = 100-900 msec), which developed after channels inactivated. The amplitude of the block during the rapid phase of development was a steep function of transmembrane voltage over the range of -70 to +20 mV. The voltage-dependence was similar to that for sodium channel activation (sodium conductance) but was too steep to be attributed solely to the passive movement of a singly charged molecule under the influence of the transmembrane voltage gradient. These results suggest that use-dependent block of sodium channels in cardiac tissue may result from an interaction of lidocaine with sodium channels in the activated as well as the inactivated channel states. Possible mechanisms underlying the fast component of block are discussed.

Original languageEnglish (US)
Pages (from-to)869-878
Number of pages10
JournalCirculation research
Issue number5
StatePublished - 1988

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology


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