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The effects of amniocentesis (Ax) on the growth and development of fetal rat lung were studied in littermate fetuses subjected to minimum (Ax-Min; 0.1 ml) and maximum volume (Ax-Max; 0.5 ml+) amniocentesis at 17 days gestation. Non-operated littermates served as controls. Lungs of 12-14 fetuses/group were analyzed at term (22 days) for weight, composition (DNA, glycogen, lipid, phospholipid, phosphatidyl-choline) and histology (light and EM). Only Ax-Max reduced the weight of the lung (p>.1). DNA content was not influenced by Ax. Both Ax-Max (p>.02) and Ax-Min (p>.1) reduced lung glycogen. Ax did not alter the quantity of lung lipid at birth. The phospholipid fraction/lung was reduced (p>.05) after Ax-Max but not Ax-Min. The lungs of Ax-Max fetuses showed reduced alveolar space size and type II pneumocytes with few lamellar bodies and little glycogen. Histologic changes were not observed after Ax-Min. These studies indicated that large volume Ax reduces lung size by obliterating the fetal lung space rather than inhibiting lung cell proliferation. Ax-Max also reduces the phospholipid and surfactant pool size. Ax-min results in few detectable changes in lung growth or development. These studies explain certain aspects of the pulmonary dysfunction of infants with prolonged oligohydramnios.