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      Effect of lidocaine on the electrophysiological properties of ventricular muscle and purkinje fibers.

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      The Journal of clinical investigation
      American Society for Clinical Investigation

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          Abstract

          Preparations of right ventricular papillary muscle and false tendon (Purkinje fiber) were obtained from dog hearts, placed in a bath perfused with Tyrode solution, and observed both under control conditions and during exposure to lidocaine in concentrations from 1 x 10(-7) to 5 x 10(-4) mole/liter. Transmembrane voltages were recorded from both ventricular muscle (VM) and Purkinje fibers (PF) of spontaneously beating and electrically driven preparations. Low concentrations (1 x 10(-6) and 1 x 10(-5) mole/liter) attenuated or abolished phase 4 (diastolic) depolarization and spontaneous firing in PF without decreasing their diastolic excitability. Concentrations of 1 x 10(-5) mole/liter produced maximal shortening of both action potential duration (APD) and effective refractory period (ERP) and made the ERP long relative to APD; the latter alteration was more prominent in VM. At concentrations </= 1 x 10(-5) mole/liter, lidocaine either caused a slight increase or no change in peak maximum rate of phase 0 depolarization (V(max)) and membrane responsiveness, the relationship between transmembrane activation voltage (MAV) and V(max) of the resultant action potential; these concentrations had no significant effect on resting potential (RP) in VM, maximal diastolic transmembrane voltage (DTMV(max)) in PF, or action potential amplitude in either fiber type. High (toxic) concentrations (>/= 1 x 10(-4) mole/liter) did not cause further shortening of APD or ERP in either VM or PF but did produce a decrease in peak V(max) of phase 0 and membrane responsiveness. In most cases, these concentrations also caused a decrease in RP or DTMV(max) and action potential amplitude, with progression to bizarre action potential depolarization and inexcitability. These properties of lidocaine are strikingly different from those of quinidine or procaine amide. The mechanisms responsible for lidocaine's in vivo antiarrhythmic action are discussed.

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          Author and article information

          Journal
          J Clin Invest
          The Journal of clinical investigation
          American Society for Clinical Investigation
          0021-9738
          0021-9738
          Jan 1970
          : 49
          : 1
          Article
          10.1172/JCI106224
          322445
          5409809
          9e563c08-0778-460f-a770-fef68515830f
          History

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