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 (VE), blood gas values, cardiac output (Q), and whole-body O2 consumption (VO2) were measured at various levels of inspired O2 concentration (FIO2) before and after denervation of carotid chemoreceptor afferents. In the carotid sinus nerve (CSN)-intact rat, the reduction in FIO2 from > 0.27 (hyperoxia) to about 0.10 (mild-moderate hypoxia) elicited an augmentation of VE which was accompanied by a well maintained total amount of O2 delivered to tissue (Q x O2 content of arterial blood, DO2) and VO2. The increase in VE was, however, turned off and the VE value did not differ from that in hyperoxia at FIO2 lower than 0.10 (moderate-severe hypoxia) (hypoxic ventilatory depression, HVD). Significant decreases in Q, DO2, and VO2 were also seen at FIO2 < 0.10. After CSN section, VE, Q, DO2, and VO2 values decreased progressively with the reduction in FIO2 from hyperoxia to mild hypoxia (FIO2 = 0.20-0.15). These findings indicate that the normal DO2 and VO2 are preserved in the presence of carotid chemoreceptor afferents in the FIO2 range > 0.10 and that HVD is accompanied by the decrease in VO2. Summarizing all results, VO2 decreased linearly with the reduction in PaO2 lower than about 60 mmHg or DO2 lower than 4 ml/min/100 g bw (critical PaO2 or DO2 for metabolic suppression), above which VO2 remained unchanged. The decrease in VO2 in lower PaO2 or DO2 levels (hypoxic hypometabolism) ensues perhaps from "adaptive" mechanisms reducing O2 demand when adequate O2 supply to tissue is limited.