Morphologic Changes of the Uteroplacental Unit in Preeclampsia-Like Syndrome in Rats

Mayr, Andreas; Lederer, Wolfgang; Wolf, H; Dünser, Martin W.; Pfaller, Kristian; Mörtl, M

doi:10.1081/prg-45770

Cited by 11 publications

(5 citation statements)

References 15 publications

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“…The present study showed no effect of L-NAME on litter size in the rat model. In contrast, a few previous studies have shown reduced the size of litter in L-NAMEinduced rats (Celadilla et al, 2005;Isler et al, 2003;Mayr et al, 2005). Furthermore, in the present study, the administration of L-NAME showed an approximately 20% decrease in pup weight, suggesting that pre-eclampsia might cause intrauterine growth retardation.…”

Section: Discussioncontrasting

confidence: 96%

TaVNS reduces inflammatory responses in a L-NAME-induced rat model of pre-eclampsia

Zheng¹,

Tang²,

Zhou³

2021

Biocell

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Pre-eclampsia is characterized by an excessive maternal inflammatory response. The cholinergic antiinflammatory pathway (CAP) has been shown as the efferent arm of a vagal reflex with the potential to limit inflammatory responses. Therefore, in this study, the CAP regulation through the nervous vagal stimulation (VNS) reduced the severity of NG-nitro-L-arginine methyl ester (L-NAME)-induced pre-eclampsia was determined in a rat model. Rats were given 125 mg/kg/day of L-NAME via subcutaneous injection on gestational day (GD) 10-16. In addition, the rats were treated by active or sham electrical stimulation once a day during GD 13-19. Systolic blood pressure (SBP), urinary albumin, and pregnancy outcomes were documented for each rat. The average fetal weights and crown-rump length (CRL) as well as the placental weights of rats in both control and experimental groups were recorded onthe 13th day, 16th day and 20th day of gestation. Subsequently, placentas were collected from the rats on GD20 to measure the level of cytokines. In addition, qRT-PCR and Western blot analysis were used to detect the mRNA and protein expression of α7 nicotinic acetylcholine receptor (α7nAChR) and nuclear factor-κB (NF-κB), respectively. Immunohistochemistry assays were also carried out to determine the location and level of α7nAChR and NF-κB in placentas. CAP regulation through the transcutaneous auricular nerve stimulation alleviated the clinical symptoms in the rats after L-NAME induction, including hypertension, proteinuria, fetal growth retardation and fetal death. In addition, TaVNS also increased α7nAChR expression, reduced NF-κB p65 expression, and reversed L-NAME-induced proinflammatory cytokines in the placenta tissues, including tumor necrosis factor-alpha (TNF-α), high mobility group box 1 (HMGB-1) and interleukin-6 (IL-6). The findings of this study showed that TaVNS might be used as a promising tool to attenuate pre-eclampsia-like symptoms. In addition, the protective effect of TaVNS was associated with the improvement of α7nAChR expression and the inhibition of inflammatory reactions at the maternal-fetal interface through activating cholinergic anti-inflammation pathway.

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Section: Discussioncontrasting

confidence: 96%

TaVNS reduces inflammatory responses in a L-NAME-induced rat model of pre-eclampsia

Zheng¹,

Tang²,

Zhou³

2021

Biocell

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“…The model of hypertension in pregnancy established in our study has been documented to be widely used to examine the maternal and fetal manifestations of preeclampsia in pregnant rats [17][18][19][20] . The present study revealed that hypertension in pregnancy led to elevated systolic blood pressure, decreased litter size [25] and viable fetuses [26] , and reduced fetal and placental weights [27] , which are similar to the deleterious changes seen in preeclamptic women [1,11] . The relative lag in placental weight suggests that there may be a compensatory mechanism such as enhanced placental transport capacity to meet the demands of the growing fetus and this phenomenon has been shown in other studies [17][18][19][20][21][22][23][24][25][26][27][28] .…”

Section: Discussionsupporting

confidence: 73%

Cardiac myeloperoxidase activity is elevated in hypertensive pregnant rats

et al. 2017

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Myeloperoxidase (MPO) is released from activated neutrophils. The inflammation in preeclampsia was found to be associated with endothelial dysfunction. We hypothesized that cardiac and circulating MPO levels are elevated in hypertensive pregnancy. Systolic and diastolic blood pressure and heart rate were measured on pregnancy days 14, 16, 18 and 20 in normal pregnant and hypertensive pregnant rats. Left and right ventricle weights, the number of viable fetuses, litter size, fetal and placenta weights were recorded on gestational day 21. Circulating and cardiac MPO activities, soluble fms-like tyrosine kinase-1 (sFlt-1) and vascular endothelial growth factor (VEGF) and nitric oxide (NO) were detected. The results showed increases in cardiac (left, but not right ventricle) and circulating MPO activities, and concomitantly lower number of viable fetuses, litter size, and fetal and placenta weights, and decreases in NO in hypertensive pregnant rats. Also, the increases in circulating sFlt-1 and VEGF were found in hypertensive pregnant group. In conclusion, maternal and fetal detrimental changes along with increases in circulating sFlt-1 and VEGF in hypertensive pregnancy may be associated with increases in cardiac and circulating MPO activities, confirming the causative role of inflammatory response in preeclampsia.

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“…However, there was no effect on the vasodilation of early pregnancy that is normal in primates including humans. The chronic NOS inhibition model during pregnancy is limited in its usefulness in pre‐eclampsia research as it offers little insight into the pathogenesis of the disease; however, it is still being used in the study of therapeutic agents and the physiological mechanisms of hypertensive pregnancies 55–58 …”

Section: Vasoconstriction Modelsmentioning

confidence: 99%

Animal Models of Pre-eclampsia

Sunderland

Hennessy

Makris

2010

American Journal of Reproductive Immunology

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The cardinal features of human pre-eclampsia, hypertension and proteinuria, are mimicked in animal models. Increasingly, the accuracy of inducing 'pure' systemic endothelial dysfunction is regarded as critical in differentiating mechanisms of pre-eclampsia from other conditions which induce hypertension (e.g. glomerulonephritis, renal denervation or manipulation of the renin-angiotensin system). A recent study in baboons has identified the timing of induction of maternal endothelial damage after acute uteroplacental ischaemia (UPI). The endothelial changes in the glomerulus are indicative of a direct endothelial toxin and mimic the lesions seen in human pre-eclampsia; the extent of hypertension and proteinuria are also similar. This animal model identifies systemic and placental sFLT-1 (soluble fms-like tyrosine kinase-1) as a potential mediator of endothelial damage. This research involving primates with haemomonochorial placentas makes translation of these results to humans very compelling for understanding the mechanisms of human disease. Similar endothelial dysfunction has been identified in baboons treated with anti-inflammatory inhibitors. Similar studies in rodents have identified a relationship between angiotensin II agonistic antibodies, UPI/reduced uteroplacental perfusion pressure, angiogenic markers, and cytokines. We can now identify vasoconstrictive mediators of the hypertensive and endothelial response such as endothelin 1, the renin-angiotensin system, or other hormones such as oestrogens in primate models.

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Morphologic Changes of the Uteroplacental Unit in Preeclampsia-Like Syndrome in Rats

Cited by 11 publications

References 15 publications

TaVNS reduces inflammatory responses in a L-NAME-induced rat model of pre-eclampsia

TaVNS reduces inflammatory responses in a L-NAME-induced rat model of pre-eclampsia

Cardiac myeloperoxidase activity is elevated in hypertensive pregnant rats

Animal Models of Pre-eclampsia

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