Figure 1.

The anapyrexic effects of hypoxia: a role for the carotid chemoreceptors. (A) The hypothermic effects of 6-h hypoxia exposure (F_iO₂ = 5%) at a T_a of 21.3 ± 0.3 °C, presented as mean ± SEM maximum superficial T_b normalized to normoxia control values (F_iO₂ of 21%) in mice (adapted from Hemelrijk et al.¹⁸). (B) Schematic overview of hypoxia sensing mechanisms by the carotid body (CB). Consequent to a hypoxic challenge by exposure to a reduced F_iO₂, the partial arterial oxygen pressure (P_aO₂) decreases and the CBs are activated. CB activation is followed by the ventilatory response (left) as well as anapyrexic signaling (right). The hypoxic ventilatory response comprises predominately an increase in respiratory rate (RR) and, to a lesser extent, an increase in tidal volume (V_T), both contributing to an increase in minute volume (V_E). Anapyrexic signaling is activated by downmodulation of the thermoneutral zone (Z_tn), which promotes a heat loss mechanism and causes a reduction in body temperature (T_b) if the surface area (SA):volume (V) ratio is large enough. Hypothermia reduces metabolism in accordance with Arrhenius’ law. The ventilatory response and anapyrexic signaling in small animals (large SA:V ratio) inhibit the decrease in P_aO₂ by improving oxygenation and reducing O₂ consumption, respectively. Isoflurane is known to influence thermoregulation by promoting heat loss mechanisms (a.o., vasodilation). Activating/stimulatory relationships between variables are depicted by arrows, inhibitory relationships by squares.