Department of Psychology and Center for Developmental Psychobiology, Stale University of New York, Binghamlon, NY 13902-6000 (U.S.A.).
Restor Neurol Neurosci. 1991 Jan 1;3(1):11-22. doi: 10.3233/RNN-1991-3102.
This study investigated the effects of fetal rat umbilical cord compression on anatomical, biochemical, and behavioral parameters of development. Further, the study examined the ability of the calcium channel antagonist nimodipine to afford protection from this insult. Near the day of birth (E21), the umbilical cord of individual fetuses was not clamped or clamped for 2, 6, or 12 min. Before clamping, mothers were given 70 μg/kg (i.p.) nimodipine in a polyethylene glycol (PEG) vehicle or the vehicle alone. Selected animals were sacrificed for cytochrome oxidase histochemistry. The remainder of the pups were given to foster mothers and allowed to develop through adulthood. At the end of testing all animals were sacrificed and the brains weighed and measured. Histochemical analysis revealed that clamping resulted in a decrease in cytochrome oxidase reaction product in the hippocampus. The reduction in this marker of oxidative metabolism was not as pronounced in animals from drug-treated mothers. Alterations in behavior produced by clamping were detectable as early as the third day after birth (P3). At this age, pups subjected to cord clamping exhibited impaired righting and diminished avoidance of a 'cliff' on which they had been placed. On P67-P75, clamped animals exhibited hyperactivity in an open field, low rates of spontaneous alternation in a T-maze, and impaired learning and memory in a Pavlovian conditioned aversion-to-brightness test. The calcium channel blocker afforded protection from the effects of cord clamping, since the nimodipine-treated animals were less impaired in these behavioral tests. Animals that had been subjected to cord clamping showed reduced brain volumes and dimensions on P80. Nimodipine treatment normalized these parameters of brain development relative to non-clamped controls. Taken together, these results indicate that brief periods of umbilical cord occlusion near the time of birth can have both immediate and long-term effects on different parameters of development. In addition, the calcium channel blocker nimodipine affords partial protection from damage induced by compression of the fetal umbilical cord.
本研究探讨了胎儿脐带受压对解剖、生化和行为发育参数的影响。此外，本研究还研究了钙通道拮抗剂尼莫地平是否具有抵抗这种损伤的能力。在接近分娩的日子（E21），单独胎儿的脐带未被夹住或夹住 2、6 或 12 分钟。在夹闭之前，母亲们在聚乙二醇（PEG）载体中接受 70μg/kg（i.p.）尼莫地平或单独载体。选择的动物进行细胞色素氧化酶组织化学分析。其余的幼仔被交给养母，并允许其成年。在测试结束时，所有动物均被处死，脑重和脑尺寸被测量。组织化学分析显示，夹闭导致海马体细胞色素氧化酶反应产物减少。来自接受药物治疗的母亲的动物中，这种氧化代谢标志物的减少并不明显。夹闭引起的行为改变早在出生后第三天（P3）就可检测到。在这个年龄，脐带受压的幼仔表现出翻身能力受损和避免放在“悬崖”上的能力下降。在 P67-P75，受压动物在开阔场中表现出过度活跃，在 T 型迷宫中自发交替率低，以及在巴甫洛夫条件性厌恶亮度测试中学习和记忆受损。钙通道阻滞剂提供了对脐带受压影响的保护，因为尼莫地平处理的动物在这些行为测试中受损程度较低。在 P80，已经受到脐带夹闭的动物的脑体积和尺寸减小。尼莫地平治疗使这些大脑发育参数相对于未夹闭的对照组正常化。总之，这些结果表明，在接近分娩时短暂的脐带阻塞期会对不同的发育参数产生即时和长期的影响。此外，钙通道阻滞剂尼莫地平可提供部分保护，防止胎儿脐带受压引起的损伤。
