Metabolic and ventilatory sensitivity to hypoxia in avian embryos.

The article discusses the establishment of pulmonary ventilation (V˙E) in the avian embryo, the metabolic and V˙E sensitivity to hypoxia and the effects of sustained embryonic hypoxia on the hatchling's V˙E chemosensitivity. Throughout embryogenesis, hypometabolism is the common response to hypoxia, with no compensation by anaerobic energy supply. It originates primarily from the depression in body growth and, later in development, from the depression of thermogenesis. The V˙E responses to acute hypoxia or hypercapnia are clearly detectable during the internal pipping phase; their magnitude rapidly increases in the first postnatal day. Sustained prenatal hypoxia diminishes the V˙E chemosensitivity of the hatchling and reduces the hypometabolic response to an acute hypoxic episode. The former most likely originates from a disturbance in the normal development of the carotid bodies, the latter from the central action of hypoxia on thermogenesis. The avian embryo is a model suitable for the studies of the development of respiratory control and offers an alternative to mammalian models for investigations on the short- and long-term effects of prenatal hypoxia.