Department of Obstetrics and Gynecology, Faculty of Medicine, Inonu University, Malatya, Turkey.
Arch Gynecol Obstet. 2012 Mar;285(3):655-61. doi: 10.1007/s00404-011-2069-5. Epub 2011 Aug 25.
The purpose of this study was to evaluate the cardiac and cerebral oxidative stress in the offspings of pregnant rats treated with oxytocin antagonist atosiban.
Experimentally naive, adult female Wistar-albino rats (200-250 g) were mated with adult male rats for copulation. After confirming pregnancy, eight gravid rats were then randomly assigned into two equal groups. The animals were treated from days 15 to 20 of gestation. One group acted as a control group, and received intraperitoneal (i.p.) injections of saline in a daily dose volume of 6 mg/kg/day. The second group received 6 mg/kg/day i.p. atosiban. On day 21 of gestation, pups were delivered by cesarean. The heart and brain tissues of the newborn rats were dissected and sent for the measurement of total oxidant status, total antioxitant status and oxidative stress index.
There was no significant difference in birthweight or in the number of pups between two groups. Newborns from atosiban-treated mothers showed significantly increased oxidative stress in the plasma and heart tissue than that of controls which was confirmed by histological examination (P < 0.05). Oxidative stress parameters and histopathological results of the brain tissues of newborns were similar between two groups (P > 0.05).
Oxytocin receptor blockage for the treatment of premature delivery may be associated with increased fetal morbidity and mortality secondary to the elevated oxidative stress in the heart of the newborns.
本研究旨在评估接受催产素拮抗剂阿托西班治疗的孕鼠后代的心脏和大脑氧化应激。
实验用成年雌性 Wistar 白化大鼠(200-250g)与成年雄性大鼠交配以进行交配。确认怀孕后,将 8 只妊娠大鼠随机分为两组。动物从妊娠第 15 天到第 20 天接受治疗。一组作为对照组,每天腹腔注射(i.p.)生理盐水 6mg/kg。第二组接受 6mg/kg/day i.p.阿托西班。妊娠第 21 天,通过剖腹产分娩幼崽。从新生大鼠中取出心脏和脑组织,并用于测量总氧化剂状态、总抗氧化状态和氧化应激指数。
两组的出生体重或幼崽数量无显著差异。与对照组相比,来自阿托西班处理的母亲的新生儿的血浆和心脏组织中的氧化应激明显增加,这通过组织学检查得到证实(P<0.05)。两组新生儿的脑组织的氧化应激参数和组织病理学结果相似(P>0.05)。
为治疗早产而阻断催产素受体可能与新生儿心脏氧化应激增加相关,从而导致胎儿发病率和死亡率增加。