An electron-microscopic study has shown that in placentae from prolonged pregnancies there is hyperplasia of the villous cytotrophoblastic cells, degeneration of occasional isolated cytotrophoblastic cells, a paucity of syncytial microvilli in some areas and microvillous proliferation in others, abnormalities of microvillous form, focal syncytial necrosis, dilatation of syncytial endoplasmic reticulum, decreased synctial pinocytic activity, a reduced size and number of syncytial mitochondira, thickening of the trophoblastic basement membrane and contraction, blebbing and vacuolation of endothelial cells of the stromal foetal villous capillaries. Many of these morphological changes indicate that there is, in prolonged pregnancy, a decline in trophoblastic functional activity but it is suggested that this is due, not to placental senescence, but to a relatively mild, sustained uteroplacental ischaemia. Although there is morphological evidence to suggest that compensatory mechanisms come into play to limit the effects on the placenta of uteroplacental ischaemia the changes in the foetal capillaries, which are of unknown pathogenesis, will result in decreased foetal perfusion of the placenta and thus restrict still further adequate materno-foetal transfer.