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Updated: Apr 8, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
PP022. An animal model for eclampsia
Background/Aims:
Eclampsia, a leading cause of maternal mortality. Little is known about the causes of eclampsia and there is no effective treatment. Development of an animal model may help to expand our understanding and may hold great potential for the design of effective treatment.
Methods:
Experimental preeclampsia model was build first, rats were received a infusion of endotoxin (LPS) (1.0μg/kg body weight) or saline solution through the tail vein during 1h on gestational day 14, blood pressure and albuminuria were measured. On gestational day 18 all experimental rats were received electric stimulation, the seizure behaviors were observed and EEG were recorded in these rats. Terminations of pregnancy were performed on day 21 of gestation, resorptions and pups birth weights were recorded.
Results:
PE model rats develop many features of human PE that correlates with bad pregnancy outcomes. Both clinical behavior and EEG records documented seizure activity developed in 100% of pregnancy rats and 58.3% of non-pregnancy rats (P=0.01). The PE model rats had a 31.25% decrease of the latency (3.3±1.4min) to evoke a full motor seizure compared with normal pregnancy rats (4.8±2.2min), and had a significant decrease contrast to non-pregnancy rats (10.6±7.1min), £¨P<0.05). EEG recordings showed seizure activities when rats had clinically generalized tonic-clonic convulsions.
Conclusion:
We described a rat model of eclampsia, were the relevant predominant features of human eclampsia.

