Regulation of Oxygen Delivery and Consumption in Anesthetized Rats during Acute Hypoxia

Physiological roles of ventilatory responses to acute hypoxia in the regulation of O₂ transport and consumption were evaluated quantitatively in halothane anesthetized and spontaneously breathing rats with or without peripheral chemoreceptor afferents. Ventilation (V_E), blood gas values, cardiac output (Q), and whole-body O₂ consumption (V_O2) were measured at various levels of inspired O₂ concentration (F_IO2) before and after denervation of carotid chemoreceptor afferents. In the carotid sinus nerve (CSN)-intact rat, the reduction in F_IO2 from >0.27 (hyperoxia) to about 0.10 (mild-moderate hypoxia) elicited an augmentation of V_E which was accompanied by a well maintained total amount of O₂ delivered to tissue (Q × O₂ content of arterial blood, Ḋ_O2) and V_O2 The increase in V_E was, however, turned off and the V_E value did not differ from that in hyperoxia at F_IO2 lower than 0.10 (moderate-severe hypoxia) (hypoxic ventilatory depression, HVD). Significant decreases in Q, Ḋ_O2, and V_O2 were also seen at F_IO2 < 0.10. After CSN section, V_E, Q, Ḋ_O2, and V_O2 values decreased progressively with the reduction in F_IO2 from hyperoxia to mild hypoxia (F_IO2 = 0.20-0.15). These findings indicate that the normal D_O2 and V_O2 are preserved in the presence of carotid chemoreceptor afferents in the F_IO2 range > 0.10 and that HVD is accompanied by the decrease in V_O2 Summarizing all results, V_O2 decreased linearly with the reduction in P_aO2 lower than about 60 mmHg or Ḋ_O2 lower than 4 ml/min/ 100 gbw (critical P_aO2 or Ḋ_O2 for metabolic suppression), above which V_O2 remained unchanged. The decrease in V_O2 in lower P^a_O2 or Ḋ_O2 levels (hypoxic hypometabolism) ensues perhaps from “adaptive” mechanisms reducing O₂ demand when adequate O₂ supply to tissue is limited.