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Infants born early with very low birth weights frequently have high amounts of sodium in their urine and an increased loss of the fluid ordinarily found between the cells, called extracellular fluid. The amount of extracellular fluid is controlled by the balance between the amount of sodium taken in and that excreted by the kidneys. Although this condition is common in preterm infants, it is difficult to assess whether this is the result of disease or a natural response in infants born too early. To determine whether infants should receive small amounts of sodium to help reduce the extracellular fluid or increased amounts of sodium to replace sodium lost by the kidneys, 20 preterm infants were evaluated. The extracellular fluid volume (ECV) and the balance of sodium (intake and output) were measured for 10 days in two groups of infants, one receiving small and the other large amounts of sodium. During the first five days following birth, the ECV, which was normally high at birth in preterm infants, was reduced in both groups, creating a net loss of sodium. Five days later, the sodium output decreased in both groups, making the sodium balance positive. The ECV increased proportionately as the infant grew. There was a lower amount of sodium found in the blood of those infants taking in low sodium. It is suggested that low-birth-weight infants can regulate the excretion of sodium, but cannot control the concentration of sodium found in the blood. The role of hormones which regulate sodium balance cannot be overlooked, although the amounts of aldosterone and vasopressin, both sodium-controlling hormones, were not significantly different in the both groups. The adjustments made by the preterm infant to regulate the amount of ECV constitute a normal physiological response to life outside of the uterus.

Chronic sequelae of neonatal hyperoxia was studied in male rats exposed to 0.96-1.0 FiO2for the first 8 days of life. At 58 days of age functional and morphologic cardiopulmonary changes were compared with controls. Right ventricular systolic pressure was measured percutaneously under anesthesia and was increased in the O2group (29.5 mm Hg ± 3.1 versus 23.2 mm Hg ± 3.5,p< 0.001). Lung and heart weights were similar between groups. Right ventricular weights however were increased in the O2group (0.197 g ± 0.023 versus 0.175 g ± 0.020, p< 0.001). Air pressure-volume curves were similar but in the O2rats saline deflation curves were shifted left and maximal fluid lung volumes were greater (14.1 ± 1.2 versus 12.0 ± 0.7 ml, p<0.001). Pulmonary arteries were perfused at 100 cm H2O with a barium-gel mixture and lungs were fixed at 25 cm H2O with formalin. Microscopic examination of lungs revealed dysplastic changes of alveolar architecture which included irregularly enlarged alveoli and incomplete alveolar septation. Morphometric studies of the lungs showed that the O2rats had an increased volume proportion of parenchyma (0.865 ± 0.020 versus 0.850 ± 0.019, p<0.05), increased mean linear intercept (72.3 urn ± 9.5 versus 53.6 /tin ± 5.0, p<0.001), decreased number of alveoli per mm2(207 ± 34 versus 319 ± 39, p<0.001) and fewer small arteries (20-200 nm) per mm2(8.7 ±1.3 versus 14.9 ± 2.4,p<0.001). The number of small arteries/ 100 alveoli was similar. We conclude that limited and specifically timed neonatal hyperoxia is associated with chronic morphologic and functional cardiopulmonary changes in the adult rat. These changes include a decrease in the number of small pulmonary arteries, elevated right ventricular pressure, and emphysema-like changes in the air spaces.