In this study we looked for additional evidence to support the hypothesis that fetal llama reacts to hypoxaemia with adaptive brain hypometabolism. We determined fetal llama brain temperature, Na+ and K+ channels density and Na-K-ATPase activity. Additionally we looked whether there were signs of cell death in the brain cortex of llama fetuses submitted to prolonged hypoxaemia. Ten fetal llamas were instrumented under general anaesthesia, to measure pH, arterial blood gases, mean arterial pressure, heart rate and brain and core temperature. Measurements were made 1h before, and every hour during 24h of hypoxaemia (n=5), imposed by reducing maternal FiO2 to reach a fetal PaO2 of about 12 mmHg. A normoxaemic group was the control (n=5). After 24h of hypoxaemia, we determined brain cortex Na-K-ATPase activity, ouabain binding, and the expression of NaV1.1, NaV1.2, NaV1.3, NaV1.6, TREK1, TRAAK and KATP channels. Brain cortex indemnity was assessed as PARP proteolysis. We found a mean decrease of 0.56 degrees C in brain cortex temperature during prolonged hypoxemia that was accompanied by 51% decrease in brain cortex Na-K-ATPase activity and by 44% decrease in protein content of NaV1.1, a voltage-gated sodium channel. These changes occurred in absence of changes in PARP protein degradation, suggesting that brain's cell death was not enhanced in the fetal llama during hypoxaemia. Taken together all these results provide further evidence to support the hypothesis that the fetal llama responds to prolonged hypoxaemia with adaptive brain hypometabolism, partly mediated by decreases in Na-K-ATPase activity and expression of NaV channels.