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Placental Dysfuction in Surami-treated Rats - a New Model for Pre-eclampsia
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Cell Biology.
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2005 In: Placenta, ISSN 0143-4004 (Print), Vol. 26, no 5, 410-418 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2005. Vol. 26, no 5, 410-418 p.
URN: urn:nbn:se:uu:diva-95573OAI: oai:DiVA.org:uu-95573DiVA: diva2:169848
Available from: 2007-03-23 Created: 2007-03-23Bibliographically approved
In thesis
1. Experimental and Clinical Studies of Oxidative Stress in Pre-Eclampsia
Open this publication in new window or tab >>Experimental and Clinical Studies of Oxidative Stress in Pre-Eclampsia
2007 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Impaired placentation and oxidative stress are proposed to play major roles in the pathogenesis of pre-eclampsia (PE). It has recently been pointed out that PE might be more than one disease and may have several different pathogeneses. This thesis describes a new animal model for PE and examines the role of oxidative stress in early respective late onset PE.

The effects of Suramin injections on day 10 and 11 of pregnancy were investigated in normal and diabetic rats of two strains (U and H), with or without additional vitamin E treatment. Suramin caused placental dysfunction in both rat strains: foetal growth restriction, increased resorption rate, reduced placental blood flow, and decreased maternal blood volume in the placenta. In the U strain Suramin also caused maternal hypertension and reduced renal blood flow. Oxidative stress in the Suramin treated rats was indicated by increased levels of isoprostane 8-iso-PGF in the placenta. Antioxidative treatment with vitamin E partly protected against the effects of Suramin. Streptozotocin-induced diabetes seemed to cause similar placental effects as Suramin, and in the diabetic rats the additional effects of Suramin were only moderate. In conclusion, Suramin-injected pregnant rats constitute a valid animal model for placental dysfunction (U and H rats) and PE (U rats).

Oxidative stress was estimated in women with early onset (≤ 32 weeks) or late onset (≥ 35 weeks) PE, in normotensive pregnant women of respective gestational length, and in healthy non-pregnant women. The ratio of PAI-1/PAI-2 was measured in serum, and the amount of isoprostane 8-iso-PGF was measured in placenta, serum, and urine. The ratio of PAI-1/PAI-2 and placental isoprostane levels were higher in women with early onset PE compared with all other groups. Serum levels of isoprostane were similar between groups. Urinary levels of isoprostane were similar in all pregnant women, but lower in non-pregnant women. These data indicate that pregnancy increases general oxidative stress, and that early onset, but not late onset PE, causes increased oxidative stress also in placental tissue. The pathogeneses of early and late onset PE are, therefore, not likely to be identical.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2007. 63 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 238
Obstetrics and gynaecology, Pre-eclampsia, Oxidative stress, Diabetes, Placenta, Rat, Antioxidants, Suramin, Vitamin E, Vitamin C, PAI-1, PAI-2, Obstetrik och kvinnosjukdomar
urn:nbn:se:uu:diva-7717 (URN)978-91-554-6826-2 (ISBN)
Public defence
2007-04-13, B 21, Biomedicinskt centrum, Uppsala, 13:15
Available from: 2007-03-23 Created: 2007-03-23 Last updated: 2013-08-30Bibliographically approved

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