Changes in respiratory control in humans induced by 8 h of hyperoxia

Abstract

In humans, 8 h of isocapnic hypoxia causes a progressive rise in ventilation associated with increases in the acute ventilatory responses to hypoxia (AHVR) and hypercapnia (AHCVR). To determine whether 8 h of hyperoxia causes the converse of these effects, three 8-h protocols were compared in 14 subjects: 1) poikilocapnic hyperoxia, with end-tidal PO(2) (PET(O(2))) = 300 Torr and end-tidal PCO(2) (PET(CO(2))) uncontrolled; 2) isocapnic hyperoxia, with PET(O(2)) = 300 Torr and PET(CO(2)) maintained at the subject's normal air-breathing level; and 3) control. Ventilation was measured hourly. AHVR and AHCVR were determined before and 0.5 h after each exposure. During isocapnic hyperoxia, after an initial increase, ventilation progressively declined (P < 0.01, ANOVA). After exposure to hyperoxia, 1) AHVR declined (P < 0.05); 2) ventilation at fixed PET(CO(2)) decreased (P < 0.05); and 3) air-breathing PET(CO(2)) increased (P < 0.05); but 4) no significant changes in AHCVR or intercept were demonstrated. In conclusion, 8 h of hyperoxia have some effects opposite to those found with 8 h of hypoxia, indicating that there may be some "acclimatization to hypoxia" at normal sea-level values of PO(2).

Effects of maternal hyperoxia with and without normocapnia in uteroplacental and fetal Doppler studies

“…Maternal oxygen treatment has been shown in fetal lambs to be associated with fetal cerebral vasoconstriction6, 7, the cause of which is unclear. High inspired oxygen concentrations have been shown to cause significant hyperventilation and thus hypocapnia in adult humans20, while hypocapnia itself is associated with cerebral vasoconstriction10, 21–24. In preterm 8‐day‐old neonates, cerebral blood flow has been shown to be even more sensitive to low CO 2 than in adults, with hyperoxygenation associated with decreased cerebral blood flow25.…”

A potential early physiological marker for CNS oxygen toxicity: hyperoxic hyperpnea precedes seizure in unanesthetized rats breathing hyperbaric oxygen

“…In addition, protracted exposure to hyperoxia stimulates ventilation in humans and animal models, a paradoxical ventilatory response known as hyperoxic hyperventilation; reviewed by Dean et al (13). Numerous studies have shown that hyperoxia induces hypocapnia secondarily to hyperventilation (4,10,30,31,35,51,54). The degree to which hypocapnic alkalosis occurs subsequent to hyperoxic ventilation, however, has recently been challenged and is currently being debated (21, 22, 28 -31).…”

Determinants of ventilation and pulmonary artery pressure during early acclimatization to hypoxia in humans

“…To obtain parameters describing peripheral and central chemoreceptor responses from these results, mathematical models of the chemoreflexes were fitted to the data. A simple first-order model (Clement & Robbins, 1993;Ren et al 2000) was used for hypoxic sensitivity, with G pO 2 the model gain, representing the peripheral chemosensitivity to hypoxia (taken to be the total chemoreflex sensitivity). A two-compartment first-order model (Pedersen et al 1999) was fitted to hypercapnia data with two gain parameters: G pCO 2 representing the peripheral chemosensitivity and G cCO 2 representing the central chemosensitivity to hypercapnia.…”

“…A simple first‐order model (Clement & Robbins, ; Ren et al . ) was used for hypoxic sensitivity, with the model gain, representing the peripheral chemosensitivity to hypoxia (taken to be the total chemoreflex sensitivity). A two‐compartment first‐order model (Pedersen et al .…”

“…The ventilatory sensitivity to hypoxia was measured using standard methodology by exposure to a 12-min square wave variation in P ETO 2 alternating between 1 min of euoxia (100 Torr) and 1 min of hypoxia (50 Torr) while P ETCO 2 was held constant at ß2 Torr above the volunteer's natural air-breathing P ETCO 2 (Ren et al 2000). There was a 5-min lead-in period (P ETO 2 = 100 Torr, P ETCO 2 = air-breathing P ETCO 2 +2 Torr) before the start of the square wave in order to allow ventilation to reach a steady level in response to the slight increase in P ETCO 2 .…”