1098 
MONITORING 
Cfl 
& 400 
S 6 
TIME (SEC) 
Figure 10. — Rate constants of return to normal size. 
of the stimulation, while the imbalance exists, 
the heart period is prolonged. 
Figure 11 represents a simulation for arti- 
ficial pacing. The top figure is the voltage across 
the membrane. In the lower left is the voltage 
across the RC circuit as stimulation progresses. 
On the right half of the figure are values for 
Eji and Eri following cessation of the pace- 
making, illustrating the fall in Eci, the de- 
pressed slope of the prepotential, the so-called 
post-pacemaker depression — a long beat and the 
slow return to control heart period. 
Further simulated acetycholine experiments 
were carried out to find the parameters of the 
equation, using the interactive graphic features. 
Each simulation ran about 15 minutes with out- 
put on the oscilloscope. Observing the wave- 
form permitted educated guessing and short- 
ened the time for solution. Extensive simulation 
experiments were then carried out perturbing 
both the potassium and sodium conductances 
with an exponential function with varying time 
constants. 
Figure 12 illustrates the results of one such 
simulation. Again the top row gives the sim- 
ulated membrane potential, the second row the 
change in potassium current simulating the 
acetylcholine pulse, and the bottom is the post- 
ulated voltage across the Eci. The features are 
a prompt inhibition, a depressed prepotential, 
and a gradual return to control period. Figure 
13 illustrates the logarithm of the period fol- 
lowing the simulated vagal inhibition, which 
resembles the data achieved by the very rapid 
initial change in the heart period in this case, 
a slope of .6 sec followed by an exponential of 
significantly greater value (2.6 seconds). The 
model also demonstrates phasic responsiveness. 
SUMMARY 
A case study has been presented in the use 
of a general-purpose, time-shared computer 
system for physiological research. The experi- 
ments used computer-controlled stimulations to 
demonstrate that the heart will lock in phase 
and frequency to a forcing vagal stimulation 
frequency. Graphics and controlled stimulation 
demonstrated that the cardiac cycle is tempo- 
rarily non-uniform in its response to brief vagal 
stimulation. Long-term storage of data, curve 
fitting, and use of statistical libraries acceler- 
ated the demonstration that there are two 
phases as the inhibited heart rate returns to a 
control state. The later phase does fit an ex- 
s = S o 8 S 8 
iiiioz 
Figure 11. — Simulation for artificial pacing. 
