73
7.37 t .01 (mean  SEM) during the control period to
7.08  .03 in Group A and an increase in Group B from
7.36  .02 to 7.52  .02. After 60-90 minutes, ventilation
was increased to 20 breaths per minute in Group A and
reduced to 3-4 breaths per minute in Group B. This
second alteration in ventilatory frequency resulted in
an increase in pH to 7.4 in Group A and a reduction in
Group B to 7.2 (see Figure 16). In Group C, ventilation
was not altered, and arterial pH did not vary during the
experiments. The reduction in ventilation did not
significantly decrease arterial PC>2 
When arterial pH remained constant for 2 hours
(Group C), AT increased with time. By the end of 2 hours,
AT was greater than it had been at the first 20 minute
period. As illustrated in Figure 17, AT increased with
time in Group A also but not in Group B. The only
significant difference in Groups A and B was that AT
during hyperventilation was greater than AT at any other
time period in Group A and greater than control in Group
B (see Table IV).
Despite the apparent effect of hyperventilation on AT,
there was no significant correlation of AT with arterial
or venous H+ concentration (see Table V). Furthermore,
AT was not reduced during hypoventilation. When arterial
pH fell to 7.09  .03, AT did not change significantly.
In Group C, dP/dt did not change significantly. In
Group A and Group B, however, dP/dt was higher during