Birthweight in a non-human primate model of placental ischaemia.

Animal models for preeclampsia are mostly determined by the experimental induction of hypertension, proteinuria and latterly, endogenous production of anti-angiogenic factors (sFlt-1). The focus on maternal outcome measures is more immediately obvious, with comparative and sequential data of blood pressure and urine protein excretion. In non-human primates, the data concerning birthweight requires a greater number of observations and thus will be accumulated over a longer period of time and a greater number of experimental protocols. The following represents the outcome of over 20 years of experimental preeclampsia (EPE) compared with normal pregnancy outcome data in baboons. MethodsThis data represents the outcomes from 91 pregnancies over the last 25 years at the Australian National Baboon Colony. These pregnancies are attributed to females who had experimental preeclampsia (EPE) and those within the general colony. EPE was induced at day 130 (of 182 days gestation length), and in some protocols, treatments such as inhibitory RNA or placental growth factor (PlGF) were tested. All studies were approved by the institutional Animal Welfare Committee. RESULTS: The overall neonatal birthweight was 697 g ± 115 g. The average birthweight for normal males was 770 ± 105 g; and for male offspring of animals with EPE, 680 ± 113 g; for normal females was 640 ± 95 g and females from EPE pregnancies, 690 ± 43 g. There was only a significant difference in weight for females compared to males overall (p = 0.002), and there was no significant difference in birthweight for males or females subjected to EPE. Correction for treated EPE did not change the outcome. CONCLUSIONS: These data indicate that in a non-human primate model of placental dysfunction through late pregnancy acute ischaemia, there is no measurable effect on baby birthweight compared to normal pregnancy, and no impact from a number of current experimental treatment strategies.