ABSTRACT

The fetal llama must cope with the low-fetal arterial PO2 of all species but also the superimposition of maternal hypoxia because of the decreased oxygen environment of the Andean altiplano. When subjected to acute hypoxia, the fetal llama displays an intense peripheral vasoconstriction mediated by alpha-adrenergic mechanisms plus high plasma catecholamine concentrations. Endothelial factors such as NO and endothelin-1 are also vital modulators in the regulation of local blood flows. Unlike fetuses of lowland species such as the sheep, the fetal llama shows a profound cerebral hypometabolic response to hypoxia, decreasing cerebral oxygen consumption, Na-K-ATPase activity, and temperature without cerebral damage. Regarding the pulmonary circulation, the neonatal llama does not have pulmonary hypertension in the highlands, having an enhanced HO-CO pathway, higher than that of the neonatal sheep at the same altitude, added to an important NO pathway during acute hypoxia. In contrast, the sheep newborns rely only on enhancement of the eNOS-NO system, with high eNOS protein expression and NO production by the lung, but these mechanisms are not sufficient to avoid newborn pulmonary artery hypertension. With all these notable strategies, the fetal and neonatal llama gracefully sway in the thin oxygen trail at the Altiplano.