Oxidative stress occurs when the production of reactive oxygen species overwhelms the intrinsic anti-oxidant defenses. At the moment it is not clear whether the observed reduction in PNO2 protein expression in the placenta in the labour group is a consequence of labour itself or, alternatively, contributed to labour via endocrine, hemodynamic or other processes. Since human patients have been used it is difficult to separate these effects. It is known however that contraction of the uterus leads to ischemicreperfusion injury that can alter placental protein expression. Furthermore Doppler ultrasound studies have demonstrated an inverse relationship between Brusatol uterine artery resistance and the intensity of uterine contractions during labour. It has been shown in chronically instrumented pregnant rhesus monkeys that placental blood flow is almost completely stopped during sustained myometrial contractions and that this occurs as a result of compression of the arcuate and spiral arteries. The closest human model to this was performed on patients prior to termination of pregnancy at weeks of gestation. During oxytocin-induced contractions, a 50% reduction in flow into the intervillous space, as well as a fall in entry sites and volume, was found compared to when no contractions occurred. This suggests that intermittent perfusion of the intervillous space would lead to an ischemic-reperfusion injury of the placenta. Reactive oxygen species and the oxidant/antioxidant balance can be affected as a result. In keeping with this labour has been reported to be associated with placental alterations in several pathways linked to oxidative stress Other studies looking at heat shock proteins, Mn-SOD, Cu/Zn-SOD and peroxidation of lipids also show an association between labour and placental oxidative stress. The biochemical events associated with labour involve increased Povidone iodine interleukin-1b and prostaglandin synthesis. The later stages of gestation are likely to be associated with more fluctuations in blood flow as demand by the placenta and fetus is maximal.