Prenatal caloric restriction in guinea pigs causes intrauterine growth retardation and reduced neonatal viability and surfactant phosopholipid (PL). We report here fetal surfactant levels in this model, and correlate total lung PL with ultrastructural maturation of surfactant type II cells and lamellar bodies (LB). Pregnant guinea pigs were fedad libitumthroughout their 68-d gestation (control), or fed 50% rations from d 45 until term (starved). Fetal lungs were examined at d 55, 60, and 65 for PL content and composition, including disaturated phosphati-dylcholine (DPC), and compared with neonates for both groups. Lung lobes were analyzed ultrastructurally in d 65 fetuses for the numerical, volume, and surface densities of type II cells and the volume densities of LB. Prenatal starvation caused significant intrauterine growth retardation at all ages; body and dry lung weights were reduced on d 65 by 26 and 23%, respectively. By d 55 and thereafter, starvation decreased total lung PL by 43–45% but did not alter PL composition. On d 65, the total lung volumes and relative numbers, surface densities, and volumes of type II cells in tissue and the relative volumes of LB within type II cells did not differ by caloric regimen. Thus, starved and control fetuses had similar total volumes of LB per lung (13–15 $mUL), although starved animals had significantly less lung DPC. Although the total volume of LB per lung correlated well with total lung DPC from d 55 through birth in controls, starvation led to a significant departure from this relationship. These results suggest that the concentration of DPC within LB can vary markedly without changing the size and appearance of the LB, or that the reduced amounts of DPC in starved fetuses represent deficiencies of surfactant from non-LB compartments. (Pediatr Res29: 288–291, 1991)