Low oxygen tension in the management of newborn infants.

Prolonged administration of oxygen in high concentrations to premature infants is now being abandoned in most countries, thanks to the studies on retrolental fibroplasia which have shown its harmful effects on the eyes. These studies have led to a revision of the indications for oxygen therapy and prompted renewed interest in its physiological bases in the neonatal period (Engle and Levine, 1955). It is well known that the arterial oxygen tension is extremely low during intra-uterine life-a condition described by Barcroft as 'Mount Everest in Utero' (Eastman, 1954). Immediately after birth, the arterial oxygen tension increases to the same value as that of the adult, i.e., 100 mm. Hg (Taylor, Govan and Scott, 1951). If the oxygen tension before birth is abnormally low as in asphyxiated infants (Eastman, 1936; Wilson, Torrey and Johnson, 1937; Rooth and Sjostedt, 1955; Montgomery, Brandfass and First, 1956) or infants delivered by caesarean section (Eastman, 1936; Smith, 1939; Watts, Henderson, Kaump and Davis, 1951; Rooth and Sjostedt, 1955), this increase will be more pronounced. These changes in the oxygen tension are known to produce important vasomotor reactions in the vessels of the brain, eyes and lungs, which in human infants are of special interest, due to the correlation between the two diseases retrolental fibroplasia and hyaline membrane and oxygen therapy. The frequent coexistence of retrolental fibroplasia and cerebral palsy as shown in the papers by Ingram and Kerr (1954) and Krause (1955) may perhaps also justify relating cerebral palsy to oxygen therapy. It has been shown in man that an increase in oxygen tension causes a constriction and a decrease a dilatation of the retinal vessels (Cusik, Benson and Boothby, 1940), and these reactions have been studied in relation to retrolental fibroplasia (Huggert, 1952, 1953, 1954 and others). In the