Animal models of preeclampsia

Podjarny, Eduardo; Losonczy, György; Baylis, Chris

doi:10.1016/j.semnephrol.2004.07.011

Cited by 80 publications

(36 citation statements)

References 116 publications

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“…Its clinical manifestations are maternal hypertension, albuminuria, liver and kidney dysfunction, fetal growth restriction and maternal and infant death in late pregnancy. 1 According to the World Health Organization's estimates of global incidence, 44 million live births are affected by PE each year, resulting in maternal deaths between 40 000 and 72 000. 2 Eclampsia is defined as the development of grand mal seizures in patients with gestational hypertension or PE.…”

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confidence: 99%

“…1,8 PE has been found to involve the activation of a large number of white blood cells, 9 and inflammatory markers, such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and C-reactive protein, were increased at least twofold in PE patients compared with non-pregnant patients. [8][9][10][11][12] (TNF)-a infusion and low-dose lipopolysaccharide (LPS) infusion have been used to establish animal models of PE by inducing systemic inflammation in pregnant rats.…”

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Increased neuronal seizure activity correlates with excessive systemic inflammation in a rat model of severe preeclampsia

et al. 2016

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Preeclampsia (PE), one of the most common disorders of pregnancy, is characterized by hypertension and albuminuria. In severe cases, PE results in eclampsia-like seizures. Studies have suggested that severe PE is related to an exaggerated systemic inflammatory response, which may increase sensitivity to seizures. In the current study, we investigated whether the seizure activity of neurons was enhanced under excessive systemic inflammation. We also sought to determine whether MgSO could reduce the effects of systemic inflammation on seizure activity after electrical stimulation in a lipopolysaccharide (LPS)-induced model of PE. In addition to pregnancy outcomes, we analyzed biochemical parameters to ascertain whether our PE model was successful. Enzyme-linked immunosorbent assay analysis revealed that the levels of inflammatory cytokines (tumor necrosis factor (TNF)-α and interleukin (IL)-1β) were significantly higher in the LPS-treated rats than in the untreated rats. After electrical stimulation, behavioral assessments showed that the LPS-treated rats that were not treated with MgSO had the shortest latency period to develop a seizure and the longest seizure duration. The electroencephalographic (EEG) recordings in the hippocampus demonstrated that this group also had the highest EEG amplitude. MgSO treatment significantly decreased both TNF-α and IL-1β concentrations, increased the latency to develop a seizure, decreased the seizure duration and shortened the EEG amplitude. These results suggest that neuronal seizure activity and systemic inflammation are increased in severe PE. In addition, MgSO treatment reduced systemic inflammation and seizure severity. We conclude that excessive systemic inflammation in PE promotes eclampsia seizures, which can be attenuated by MgSO treatment.

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Increased neuronal seizure activity correlates with excessive systemic inflammation in a rat model of severe preeclampsia

et al. 2016

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“…Although the etiology and pathology remain largely unknown, vascular endothelial dysfunction is the pivotal pathology of preeclampsia (1,2). The administration of L-NAME in pregnant rats represents an excellent animal model suitable for the study of cardiovascular dysfunction in preeclampsia (13)(14)(15). Vascular tone is tonically regulated by locally produced nitric oxide originating from endothelial cells.…”

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confidence: 99%

Vascular Endothelial Growth Factor Attenuates Nω-Nitro-L-Arginine Methyl Ester-Induced Preeclampsia-Like Manifestations in Rats

Chen

Wang

Huang

et al. 2008

Clinical and Experimental Hypertension

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“…Placental ischemia induced by mechanical constriction of the uterine arteries or aorta produces hypertension, proteinuria, and, variably, glomerular endotheliosis in several animal species. 13 However, placental ischemia alone, as seen in many cases of intrauterine growth restriction, does not appear to be sufficient to produce preeclampsia.…”

Section: Abnormal Placentation In Preeclampsiamentioning

confidence: 99%