EFFECT OF HYPOXIC SENSITIVITY ON DECAY OF RESPIRATORY SHORT-TERM POTENTIATION

In normal conscious humans, when a brief hypoxic ventilatory stimulus is followed immediately by breathing 100% O-2, ventilation during hype roxia gradually declines to baseline prehypoxic levels without an unde rshoot. During the decline, ventilation is greater than baseline in th e absence of hypoxia and hypercapnia. This has been interpreted as evi dence of decay of short-term potentiation (STP) or afterdischarge. It is not known whether the intensity of the stimulus that activates STP influences the time course of its decay. Therefore we studied STP deca y in nine normal adults after administration of placebo (P) and almitr ine (A) in a single-blind manner on 2 separate days. On each day, thre e runs consisting of 45 s of isocapnic hypoxia (end-tidal PO2=55 mm Hg ) followed by 2 min of hyperoxia were conducted while ventilation (VI) was measured breath by breath. Baseline VT did not differ between A a nd P, but at the end of hypoxia, VI with A was 169 +/- 14% (SE) of bas eline while VI with P was 132 +/- 7% of baseline (p<0.05). Immediately after hyperoxia was instituted, VI fell abruptly, the fall being 36% of baseline for A and 15% for P. This probably represented the withdra wal of peripheral chemoreceptor input. Thereafter, VI declined slowly toward baseline, and the time course of this decline did not differ be tween P and A. Our results indicate that within the limits we studied, the increase of the intensity of the discharge of the peripheral chem oreceptors during hypoxia does not influence STP decay.