Evaluation of oxidative/nitrative stress and uterine artery pulsatility index in early pregnancy.

INTRODUCTION: Increased oxidative/nitrative stress is characteristic not only in pathologic, but also in healthy pregnancy. High uterine artery pulsatility index (UtAPI) at the end of the first trimester is associated with altered placentation and elevated risk for adverse pregnancy outcomes. We aimed to examine the relationship of systemic oxidative/nitrative stress and uterine artery pulsatility index in the first trimester and their correlation to pregnancy outcomes. MATERIAL AND METHODS: Healthy pregnant women were recruited at 12-13th gestational week ultrasound examination; UtAPI was determined by color Doppler ultrasound. Patients were divided into high (UtAPI ≥ 2.3) (n = 30) and low (n = 31) resistance groups, and pregnancies were followed until labor. Systemic oxidative/nitrative stress was estimated by measuring total peroxide level, total antioxidant capacity and nitrotyrosine level. RESULTS: Plasma total peroxide level was significantly lower (2,510 ± 39 µM vs. 2,285 ± 59 µM), total antioxidant capacity was higher (781 ± 16 mM CRE vs. 822 ± 13 mM CRE) in the high UtAPI group, which were accompanied by lower birth weight (3,317 ± 64 vs. 3,517 ± 77 g, P < 0.05). Plasma total peroxide level showed a negative correlation (by Pearson) to UtAPI (P < 0.01) and positive correlation to birth weight (P < 0.05). CONCLUSIONS: According to our results, lower systemic oxidative stress showed correlation with high UtAPI measured between the 12-13th weeks of gestation. We also found significant differences in the birth weight of healthy newborns; therefore it is worth examining this relationship in pathological pregnancies.

Estrogen improves impaired musculocutaneous vascular adrenergic reactivity in pharmacologically ovariectomized rats: a potential peripheral mechanism for hot flashes?

Hot flashes are among the most common complaints of perimenopausal women. Despite the high prevalence of the phenomenon, the background to the development of hot flashes is still not completely understood, through a hypothesized central mechanism, involving norepinephrine and luteinizing hormone-releasing hormone (LH-RH) secretion is widely accepted. We studied the influence of sex steroid deficiency and hormone replacement therapy on the biomechanical properties of musculocutaneous arterioles, to see whether a peripheral mechanism also exists in the development of hot flashes. Fifty adult, nulliparous, non-pregnant female Sprague-Dawley rats received pharmacological ovariectomy, and estradiol, medroxyprogesterone, or both hormones. After 12 weeks the saphenous artery was isolated by microdissection. Norepinephrine-induced tone (active tangential strain) was measured as a function of intraluminal pressure in an organ bath. The norepinephrine-induced arterial tone was significantly different between the control group and the ovariectomized animals in the range of 80-150 mmHg intraluminal pressure (p < 0.05). Also, significant differences were found between the ovariectomized group and the animals receiving estradiol monotherapy (p < 0.01 between 80 and 170 mmHg, and p < 0.05 between 180 and 200 mmHg intraluminal pressure). Neither medroxyprogesterone monotherapy nor combined hormone replacement therapy induced significant changes in the norepinephrine-induced vascular tone. The absence of sex steroids leads to decreased reactivity to norepinephrine in small musculocutaneous arteries, while chronic estradiol replacement therapy restores the impaired responsiveness of the vessels. Our data raise the possibility that in addition to the central mechanism, a previously unknown peripheral background mechanism for perimenopausal hot flashes may exist.