In recent years, a substantial research effort within the specialty of pediatric surgery has been devoted to improving our knowledge of the natural history and pathophysiology of congenital diaphragmatic hernias (CDH) and pulmonary hypoplasia (PH). However, the embryological background has remained elusive because certain events of normal diaphragmatic development were still unclear and appropriate animal models were lacking. Most authors assume that delayed or inhibited closure of the diaphragm will result in a diaphragmatic defect that is wide enough to allow herniation of the gut into the fetal thoracic cavity. However, we feel that this assumption is not based on appropriate embryological observations. To clarify whether it was correct, we restudied the morphology of pleuroperitoneal openings in normal rat embryos. Shortly before, a model for CDH and PH had been established in rats using nitrofen (2,4-di-chloro-phenyl-p-nitrophenyl ether) as teratogen. We used this model in an attempt to answer the following questions: (1) When does the diaphragmatic defect appear? (2) Are the pleuroperitoneal canals the precursors of the diaphragmatic defect? (3) Why is the lung hypoplastic in babies and infants with CDH?