Abstract

Eclampsia is diagnosed in preeclamptic patients who develop convulsions and/or unexplained coma during pregnancy or postpartum. It is one of the leading causes of maternal and infant morbidity and mortality accounting for about 13% of all maternal deaths worldwide. While several factors contributing to the pathogenesis of preeclampsia have been identified, little is known about the mechanisms contributing to the pathophysiology of eclampsia, partly due to the lack of suitable animal models of eclampsia. The aim of this study was to test the hypothesis that placental ischemia, induced by reducing utero-placental perfusion, increases susceptibility to seizures and cerebral edema. Pentylenetetrazol (PTZ), a pro-convulsive drug, was injected into pregnant and placental ischemic rats (40 mg/kg, i.p.) on gestational day 19 followed by video monitoring of rats for seizure activity for a duration of 30 minutes. Seizure scoring was blindly conducted. Results indicate the placental ischemic rats (n=8) have reduced latency to first seizure (264.5 ± 78.7s) compared to normal pregnant rats (n=7) (835.7 ± 246.6s; p < 0.05). Placental ischemia increased brain water content in the cerebrum (78.8 ± 0.1%) compared to the normal pregnant group (78.4 ± 0.1%; p < 0.05) while PTZ treatment significantly increased brain water content in both the pregnant (78.8 ± 0.1%; p < 0.05) and placental ischemic group (78.9 ± 0.1%; p < 0.01). These data demonstrate that placental ischemia is associated with increased susceptibility to seizures and edema formation; thus the rat model of placental ischemia represents an excellent model for studying mechanisms of eclampsia-like symptoms. Further studies are required to elucidate the exact mechanisms contributing to increased seizure susceptibility following placental ischemia.

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