OBJECTIVE: Uteroplacental hypoxia is one of the proposed pathogenic mechanisms in preeclarnpsia. In a recently characterized rat model of preeclampsia, hypertension was produced by nitric oxide synthase (NOS) inhibition. Since nitric oxide deficiency may have resulted in Uteroplacental vasoconstriction, our objective was to determine if the hypertension can be reproduced by Uteroplacental ischemia. STUDY DESIGN: Varying degrees of ischemia were produced by ligating different blood vessels supplying the uterus on day 17 of gestation. Six groups (n = 6 in each group) had either the uterine only (Ua), ovarian only (Oa) or both vessels ligated on the left only (-L) or on both sides (-I.R). The ovarian suspensory ligament was ligated bilaterally in all groups. Two control groups were included, one with ligation of the ovarian suspensory ligaments (CTROSL) and one with a sham operation without ligation of any vessels (CTRSHAV1). Blood pressure (BP) was measured on day 17 prior to surgery and then daily using the tail cuff technique. The rats were sacrificed on day 22 and their uterine horns were examined. RESULTS: All rats in the (Ua + Oa)-LR group died within 3 days of surgery. Almost all the pups in the Oa-LR group aborted. Of the remaining groups, the pup weights in descending order were (Oa + Ua)4. > Ua-L > Oa-L = CTROSL = CTRSHAM. Ligation of the ovarian and/or uterine vessels resulted in similar or lower BP compared to either controls. CONCLUSIONS: Ligation of the uteroplacental vasculature reproduced the intrauterine growth restriction, but not the hypertension, seen with NOS inhibition in the pregnant rat. Uteroplacental ischemia does not produce a preeclampsia-like condition in the rat.
|Original language||English (US)|
|Journal||Acta Diabetologica Latina|
|Issue number||1 PART II|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism