The fetal llama has walked for millions of years by the thin oxygen trail of the Andean altiplano. We hypothesise that a pool of genes has been selected in the llama (Lama glama) that express very efficient mechanisms to withstand hypoxia. The fetal llama submitted to acute hypoxaemia responds with an intense peripheral vasoconstriction which is 4-5 times greater that than found in fetal sheep. This intense peripheral vasoconstriction is not changed by section of the fetal carotid sinus nerves (Llanos et al. 2003). Therefore, the response is not mediated by a chemoreflex; instead endocrine and local vascular factors play a major role. We have reported that in the fetal llama, vasopressin, neuropeptide Y, adrenaline and noradrenaline plasma concentrations are greater than those measured in fetal sheep during acute hypoxaemia (Llanos et al. 2003). In contrast, angiotensin II does not rise significantly. Alpha adrenergic blockade during acute hypoxaemia abolishes femoral vasoconstriction in both llama and sheep fetus, but prevents fetal survival in the llama fetus (Llanos et al. 2003). Local endothelial factors, such as nitric oxide (NO) provides an important vasodilator tone to brain, adrenal, kidney, gut and carcass vascular beds during normoxaemia and hypoxaemia. Interestingly, adrenal blood flow does not increase during hypoxemia in fetal llamas treated with L-NAME, an inhibitor of nitric oxide synthase (Llanos et al. 2003). Treatment with BQ-123, an inhibitor of endothelin-A receptor, does abolish the marked increase in femoral vascular resistance observed during hypoxemia in the llama fetus (Llanos et al. 2003). In the brain, there is little or no increase in cerebral blood flow during acute hypoxaemia in the llama fetus, decreasing brain oxygen delivery pari passu with the the decrease in carotid artery O₂ content. In spite of this lack of increase in brain blood flow, there is no increase in O₂ extraction across the brain, therefore a decrease in cerebral oxygen uptake occurs during different degrees of hypoxaemia in the llama fetus (Llanos et al. 2003). The fetal electrocorticogram (ECoG) mirrors this substantial reduction in cerebral oxygen consumption, since it remains flat during a 40 min hypoxemic insult, returning to normal during the immediate (60min) and late (48h) post-hypoxaemic periods (Llanos et al. 2003). With a more prolonged hypoxaemia (24h), there is a decrease in the fetal brain temperature with a reduction in activity of the Na⁺/K⁺ATPase in the cerebral cortex. Therefore, we propose that the the fetal llama brain responds to hypoxia with a marked hypometabolism. The neonatal llama also responds to acute hypoxaemia with an intense femoral vasocostriction, as intense as in the fetal life. The sensitivity to noradrenaline of the small femoral arteries is greater in the neonatal llama compared to the newborn sheep, explaining partially the intense femoral vasoconstriction observed in the former. In the pulmonary circulation, the neonatal llama has the same basal pulmonary arterial pressure in high altitude (HA) (3,580m) and in low altitude (LA) (Herrera et al. 2004). In contrast, the newborn lamb in HA has pulmonary hypertension, with the pulmonary arterial pressure 80% higher than at sea level. Clearly there is in the llama an important adaptation of the pulmonary circulation to the chronic hypoxia found in the Andean altiplano. We observed no increase in brain blood flow, but a reduction in brain oxygen uptake, decrease in Na⁺/K⁺ATPase activity cerebral cortical cells in the llama fetus. Furthermore, the fetal and neonatal llama respond to hypoxemia with an intense peripheral vasoconstriction. These responses are different from those present in lowland species and could be explained by a profound hypometabolism, both in the brain as well as the in the whole body. How this hypometabolism is produced and how the cells are preserved during this condition remains to be elucidated.