This mechanism might explain the different findings of lower fetal blood levels of amino acids transported by system A in IUGR pregnancies compared to normal levels in preeclamptic pregnancies. Several trials have explored the potential effect of prophylactic LMWHs or ASA in improving pregnancy outcome in women with thrombophilia or previous pregnancies that have been complicated by miscarriage, IUGR, preeclampsia, placental abruption, or sudden Nalidixic acid sodium salt intrauterine death. To date only ASA started before 16 weeks of pregnancy has been proven to have beneficial effects and reduces the risk for perinatal death, preeclampsia and IUGR. Despite increasing use in pregnancy the interaction between placental nutrient transfer as a feature of placental function and these anticoagulants has not been studied. The second goal of our study was therefore to explore the effect of LMWHs and ASA on placental amino acid transport under low oxygen conditions that simulate placental pathology. Concentrations of the agents chosen for this study reflect therapeutic and supra-therapeutic plasma levels of the respective substances during treatment in vivo according to previous studies. To our knowledge this is the first study to explore the effect of the anticoagulants dalteparin and ASA on placental system A and L transport. Kinetic studies using a model of isolated perfused cotyledons taken from placentae of aspirin-treated pregnancies showed that L-arginine is transported with a MMPIP significantly higher affinity, but with a lower capacity than in the non-treated group. The latter finding suggests that ASA would facilitate the uptake of the nitric oxide precursor only at very low arginine concentrations. A significant decrease in histidine transport has also been reported after aspirin treatment in rat intestine. In the few studies available, that explored the effects of hormones or drugs on placental amino acid transport, it has been reported that system A activity was stimulated by insulin, dexamethasone and glucagon in cultured human trophoblast cells.