Electrophysiological effects of lactates in mammalian ventricular tissues.
Effects of excessive lactates on electrophysiological parameters of Purkinje and ventricular muscle fibers, excised from dog hearts, were studied by the microelectrode technique. The application of 60mM-lactic acid produced the following changes in membrane potentials in both tissues: slight depolarization of resting potentials of 7 to 8 mV; decrease in the max.dV/dt of action potentials by an average of 10% from the control value; and shortening of action potential durations as well as of effective refractory periods by 17%. These effects appeared earlier in the Purkinje fibers than in the ventricular muscle fibers. The voltage dependence, max.dV/dt, was not changed after the lactate perfusion. This pointed to the depolarization of the resting potential as a cause of the decrease in the max.dV/dt of action potentials. In the Purkinje fibers, slow diastolic depolarization became manifest after the lactate application. Excessive lactates moderately depressed the slow response activity in both tissues. The perfusion of 60 mM-Na lactate had essentially similar effects in both tissues. In the ventricular muscle fibers, the voltage clamp experiments revealed that excessive lactate decreased the slow inward current and barely affected the steady-state K current. The results indicate that excessive lactates promote conditions likely to lead to a re-entry into the ventricle and, at the same time, to enhance the ectopic impulse formations in ventricular conducting tissues.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D004285:Dogs; D004594:Electrophysiology; D006321:Heart / Q000187:drug effects*; D007773:Lactates / Q000494:pharmacology*; D008839:Microelectrodes; D011690:Purkinje Fibers / Q000187:drug effects; D012032:Refractory Period, Electrophysiological / Q000187:drug effects
D007773:Lactates