抄録
(1) Hypoxia resulted in an initial (10 to 24%) decrease in diastolic threshold followed, after a period of one-half hour or more, by a progressive elevation of threshold. Reversal to a normal level of excitability occurred on readmission of oxygen.
The drive-response (D-R) interval initially shortened and then became prolonged in hypoxia but these effects were less reversable.
Refractoriness was only slightly prolonged by hypoxia.
(2) Respiratory acidosis prolonged the D-R interval and increased diastolic threshold initially. Despite continuation of CO2 excess these effects tended to diminish as though compensatory changes occurred. On restoration of normal respiration the decrease in threshold overshot the norm. Refractoriness changed but little in the entire procedure.
Rapid increase in CO2 tension produced greater changes than did gradually induced acidosis.
(3) Rapidly produced metabolic acidosis caused A-V block at about pH 7.30, but with slow infusion of ammonium chloride the pH fell lower before block occurred.
Changes in diastolic threshold were biphasic, an initial decrease was followed by a rise before block occurred. The refractory period was significantly prolonged.
