CARDIAC TRANSAIEMBRANE POTENTIALS— HOFFMAN 325 



then incrt^ase in membrane resistance simnltancdus with the action potential. If one 

 employs fluids containing only sodium or only pcjtassium outside the fiber, one can 

 get some information as to whether or not the increased conductance results from a 

 change in sodium or potassium permeability. P'urthermore, tracer studies have pro- 

 vided fairly good quantitative evidence of transmembrane ionic fluxes. However, 

 I would not want to imply that other types of transport are excluded. I think that 

 the metabolic extrusion of sodium against its electrochemical gradient and uptake 

 of potassium are both largely dependent on energy-yielding reactions in the cell, 

 and both are decreased very markedly by low temperature and by metabolic poisons. 

 On the other hand the inrush of sodium during depolarization and the efiflux of 

 potassium during recovery seemed to be influenced only slightly by metabolic 

 poisons, anoxia, or changes in temperature. 



Dr. J. W. Sevcrmghaus: I wanted to ask whether acetylcholine slowed the de- 

 polarization of pacemaker tissues the way one might expect. 



Dr. Hofjman: As far as I know there are only two major effects of acetylcholine 

 on these cardiac transmembrane potentials. In the case of the auricular muscle the 

 rate of repolarization is greatly enhanced by acetylcholine. In the case of auricular 

 pacemakers the slow diastolic depolarization is decreased. In addition, in certain 

 cases when the resting potential is low, acetylcholine may restore it to normal values. 



Dr. D. Diirrer: In experiments on the excitability of the ventricular myocardium 

 we have tried to investigate the individual roles which the anode and cathode are 

 playing. When we investigate the cardiac excitability in the ordinary way we have 

 the same results as Dr. Brooks has demonstrated. 



However, we have a set-up which makes it possible to investigate the role of the 

 anode and cathode separately. In an ordinary injection needle with a diameter of 

 0.9 mm., 10 or more small terminals are mounted so they are completely insulated 

 from each other and from the shaft of the needle. Two of these small terminals are 

 used as stimulating electrodes when the needle is applied to the ventricular myo- 

 cardium. The terminals lying between the two electrodes are used for the detection 

 of the point of origin of the extrasystolic beat. A bipolar lead is established by 

 using two terminals close to the cathode electrode and another two are chosen close 

 to the anode electrode. The first set tells what the cathode is doing, the second set 

 what the anode is doing. Both bipolar complexes have the same polarity if the 

 extrasystolic beat originates from cathode stimulation, and have the opposite 

 polarity when the activation wave comes from the opposite direction, i.e. the anode. 



With this method we believe we have proved that the strength/interval curve for 

 stimuli delivered by the two electrodes in contact with the ventricular myocardium 

 consists of two parts : an F part before the dip, which is of anodal origin, and a 

 cathodal part after the dip. 



In this way it was found that shortly after the absolute refractory period ex- 

 citability response to anodal stimuli is maximal, and diminshes in the later part of 

 the cycle. The excitability response to cathodal stimuli drops abruptly after the end 

 of the absolute refractory period to attain gradually a constant diastolic level in 

 25-40 milliseconds. 



The absolute refractory period (A.R.P.) for anodal stimulation of a region is 



