Table 1.
Physiological parameters in models of normal pregnancy (Late-Preg) and severe preeclampsia (RUPP+HC).
Figure 1.
Effect of severe preeclampsia and magnesium sulfate (MgSO4) treatment on seizure threshold and susceptibility.
(A) Representative EEG tracing during timed-infusion of pentylenetetrazole (PTZ). Black arrows indicate when PTZ infusion begun and the onset of spike-wave discharges, or seizure onset. (B) Seizure threshold was significantly lower in rats with severe preeclampsia (RUPP+HC), and treatment with MgSO4 (RUPP+HC+MgSO4) significantly increased seizure threshold back to late-pregnant (Late-Preg) control levels. (C) Rats with severe PE had significantly higher seizure susceptibility scores compared to Late-Preg controls that were reversed in RUPP+HC+MgSO4 rats. * p<0.05 vs. Late-Preg; ∧ p<0.01 vs. RUPP+HC+MgSO4; ** p<0.01 vs. all groups by one-way ANOVA with post-hoc Bonferroni test.
Table 2.
Assessment of seizure severity in late-pregnant (Late-Preg) rats, rats with severe preeclampsia (RUPP+HC), and severe preeclamptic rats treated with magnesium sulfate (RUPP+HC+MgSO4).
Table 3.
Physiological parameters of late-pregnant (Late-Preg) rats, rats with severe preeclampsia (RUPP+HC), and severe preeclamptic rats treated with magnesium sulfate (RUPP+HC+MgSO4) under chloral hydrate anesthesia for seizure threshold measurements.
Figure 2.
Effect of severe preeclampsia and magnesium sulfate (MgSO4) on seizure-induced vasogenic edema formation.
Percent water content of the posterior cerebral cortex was significantly lower after seizure in rats with severe preeclampsia (RUPP+HC) compared to late-pregnant (Late-Preg) control rats. Treatment of severe preeclamptic rats with MgSO4 (RUPP+HC+MgSO4) did not affect brain water content after seizure. * p<0.05; ** p<0.01 vs. Late-Preg by one-way ANOVA with post-hoc Bonferroni test.
Figure 3.
Effect of severe preeclampsia and magnesium sulfate (MgSO4) on in vivo blood-brain barrier (BBB) permeability to different sized solutes.
(A) BBB permeability to sodium fluorescein was increased in rats with severe preeclampsia (RUPP+HC) in the posterior cerebral cortex compared to late-pregnant (Late-Preg) control rats. MgSO4 treatment in rats with severe preeclampsia (RUPP+HC+MgSO4) had no effect on BBB permeability to sodium fluorescein. (B) Permeability of the BBB to 70 kDa Texas red dextran was similar between Late-Preg and RUPP+HC rats with and without MgSO4 treatment. * p<0.05 vs. Late-Preg by one-way ANOVA with post-hoc Bonferroni test.
Figure 4.
Effect of severe preeclampsia and magnesium sulfate (MgSO4) treatment on microglial activation.
(A) Illustration of morphological changes occurring as microglia progress from their inactive state 1, marked by long ramified processes to their active state 4, indicated by a large, amoeboid-like shape. (B) Representative photomicrographs of microglial cells stained for ionized calcium-binding adapter molecule 1 (Iba1) in the posterior cerebral cortices of late-pregnant (Late-Preg) rats, rats with severe preeclampsia (RUPP+HC) and rats with severe preeclampsia treated with MgSO4 (RUPP+HC+MgSO4). (C) The number of Iba1+ microglia was similar between groups. (D) The percentage of microglia in active state 4 was significantly higher in RUPP+HC rats compared to Late-Preg controls. Treatment of RUPP+HC rats with MgSO4 decreased the percentage of cells that were active and was similar to Late-Preg controls. ** p<0.01 vs. Late-Preg and RUPP+HC+MgSO4 by one-way ANOVA and post-hoc Bonferroni test.
Figure 5.
Effect of severe preeclampsia on cerebral blood flow (CBF) autoregulation and vasogenic edema formation.
(A) Relative CBF (rCBF) increased similarly between late-pregnant (Late-Preg) and rats with severe preeclampsia (RUPP+HC) as arterial blood pressure was increased between 100 mmHg to 180 mmHg demonstrating intact autoregulation of CBF that was not different between groups. (B) Percent water content of the posterior cerebral cortex after CBF autoregulation measurements was similar between Late-Preg and RUPP+HC rats.