Effects of anoxia and metabolic inhibitors on reaction of the fast sodium system.
The effects of anoxia and metabolic inhibitors on inactivation and reactivation of the fast Na system of dog ventricular muscle fibers were studied by examining (dV/dt)max of the action potential upstroke. Anoxia for 60 min, dinitrophenol (DNP) (2.0 mM), and sodium azide (2.0 mM) depressed markedly steady-state (dV/dt)max at each membrane potential produced by changing [K]o. Anoxia tended to prolong recovery slightly, but DNP and azide changed little the time course of recovery of the (dV/dt)max, which was studied by applying double pulses to elicit action potential at different intervals. It is concluded that anoxia, DNP, and azide caused prominent depression of the maximum Na conductance but had less influence on its recovery kinetics.
D000818:Animals; D001386:Azides / Q000494:pharmacology*; D004140:Dinitrophenols / Q000494:pharmacology*; D004285:Dogs; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles / Q000187:drug effects; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D012964:Sodium / Q000378:metabolism*; D016276:Ventricular Function
D001386:Azides; D004140:Dinitrophenols; D012964:Sodium