CELLULAR ELECTROPHYSIOLOG V OF THE HEART 



261 



Sxa and the voltage at which £,i is maximum that 

 were used in this calculation. Nevertheless, this high 

 value of gNa is not unexpected since Purkinje fibers 

 are specialized for fast conduction. 



ACTIVATION AND INACTIVATION OF SODIUM CONDUCT- 

 ANCE. VVeidmann (127) used an ingenious technique 

 for studying the kinetics of the system carrying Na+ 

 in Purkinje fibers. Two closely spaced, intracellularly 

 placed microelectrodes were used to clamp £ for a 

 short distance around them. The \oltage measured 

 with one electrode was used to control the flow of 

 current through the other. S was clamped at some 

 value for about 50 msec. The clamp was then re- 

 leased and the tissue was stimulated to produce an 

 extrasystole. The Sd of the extrasystole was then taken 

 as a measure of gNa, since the voltage at which 8,j 

 was maximum was quite independent of the clamping 

 voltage. By plotting Sd against the prespike clamping 

 \oltage, Weidmann obtained an approximation to 

 the curve relating available gNa to 8 — i.e., the relation- 

 ship between h and 8 described by Hodgkin & 

 Huxley (59). Figure 17 shows plots of Weidmann's 

 measurements of these quantities in Purkinje fibers 



bathed in solutions with normal and 25 per cent of 

 normal [Na+]. The curves are practically identical 

 in shape to those for squid axons, activation being 

 maximal for S < — 90 mv and nearly zero for 8 > 

 — 50 mv. Increasing [K+]o fivefold did not alter this 

 relationship. The time constant of activation was 

 measured by a two-step function technique like 

 that used by Hodgkin & Huxley (59). Although the 

 results are not quantitatively reliable, they are re- 

 markably similar to those obtained on squid axon. 

 Weidmann also found that action potentials initiated 

 during late repolarization or slow diastolic depolariza- 

 tion had rates of rise that varied with the membrane 

 voltage at which they were initiated in the same 

 manner as these rates did when the voltage was 

 clamped. There was, however, some time displace- 

 ment of the 8d,8 curves of potentials initiated during 

 repolarization or diastolic depolarization. He at- 

 tributed this displacement to the lag in inactivation- 

 activation equilibration behind 8 at times when 

 8 is changing. Thus it can be concluded that the 

 detailed kinetics of the changes in gxa during the 

 rising phase are much the same in Purkinje tissue 

 as in the squid axon. 



£d Lfjg.iU 



(V/Sec.) 



100% fNo% 



600 



400- 



200 



25% iNoVg 

 h x«-») 



_L 



^ 1 FIG. 18 

 (mV) 







-50 



-100 I 



25 % [k V 



-120 



-80 



-60 



-100 

 e (mV) 



FIG. 1 7. Effects of initial transmembrane potential on the 

 rate of rise of the action potential in ungulate Purkinje cells. 

 .^ local region of the membrane was clamped at a fixed voltage 

 by using an intracellular electrode measuring transmembrane 

 potential to control the current flowing from a nearby intra- 

 cellular electrode. After the membrane was maintained at the 

 potential (8, mv) indicated on the abscissa for 50 msec, the 

 clamp was released and the tissue was stimulated. The maxi- 

 mum rate of rise of the resulting action potential (Sd, v/sec) 

 was then measured and plotted as the ordinate. Reduction of 

 [Na-'']o to 25% of normal reduced the £d at any voltage but 

 did not alter the shape of the curve. Circles and crosses ; ex- 



05 



TIME (Sec) 



1.0 



perimental points; solid curves: graphs of the equation E,i = 

 (£d)i2o/(i -I- exp (S — Sh)/5), where (£d)i2ois Sd at S = —120 

 and £h is the value of h at which Ed = 0.5 (Ed)i2o. Compare 

 with curve of h vs. (S — Er) in fig. 12. [After Weidmann (127).] 

 FIG. 18. Effects of changes in the concentration of potas- 

 sium in the solution perfusing a frog ventricle on the trans- 

 membrane potentials of a single ventricular cell. Heart was 

 stimulated at time zero. Number by each curve gives per- 

 centage of the [K+]„ which is normally present in the perfusion 

 fluid. Superposed tracings of records obtained when [K''-]o 

 had the indicated value. Note effects of [K+]„ on both resting 

 and action potentials. [After Brady & Woodbury (3).] 



