ABSTRACTSThe effects of a maternal protein-calorie malnutrition during gestation and lactation were analyzed on fetal and postnatal lung growth and maturation, including a surfactant fraction isolated from lung tissue. There was a considerable reduction in body weight and in wet and dry lung weight of malnorished pups. Lung protein and DNA concentrations were similar in both groups except in late gestation (lung hyperplasia) and 2 and 15 d after delovery (hypocellularity). Lung glycogen breakdown was slowed down in malnourished newborns. Surfactant material was decreased the most perinatally and the reduction was more marked than for the nonsurfactant fraction of the lung. Disaturated phosphatidylcholine, the major surface active surfactant component, was decreased the most at birth (1.70 ± 0.31 nmol/mg wet wtversus3.68 ± 0.17 nmol/mg in controls, n = 8) and on d 2 (5.04 ± 0.53 nmol/mgversus7.67 ± 0.44 nmol/mg in controls,n= 8). There was an apparent recovery in the composition of surfactant in malnourished rats 5 d after delivery, due in fact to a decrease in controls, and an actual return to normal levels 15 to 20 d after birth. Postnatal lipid supplementation with Intralipid led to partial recovery on d 10. Inositol supplementation totally reverted the effects of malnutrition on surfactant phospholipids (8.36 ± 0.94 nmol disaturated phosphatidylcholine/mg wet wt on d 2versus7.67 ± 0.44 nmol/mg in controls and 5.55 ± 0.62 nmol/mg in untreated malnourished rats,n= 10; 2.43 ± 0.32 nmol disaturated phosphatidylcholine/mg wet wt on d 10versus3.26 ± 0.32 nmol/mg in controls and 1.18 ± 0.27 nmol/mg in untreated malnourished rats,n= 8). It is concluded that protein-calorie malnutrition profoundly affects surfactant phospholipid biosynthesis in the perinatal period and that inositol may represent a useful additive to the diet of malnourished neonates for the correction of pulmonary abnormalities. (Pediatr Res31: 629–635, 1992)