Dynamic ventilatory responses in rats: normal development and effects of prenatal nicotine exposure
Dynamic ventilatory responses in rats: normal development and effects of prenatal nicotine exposure
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DOI：
10.1016/s0034-5687(99)00054-7
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发表时间：
1999-09-01
期刊：
影响因子：
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通讯作者：
Carroll, JL
中科院分区：
文献类型：
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作者：
Bamford, OS;Carroll, JL
吸烟母亲的婴儿患SIDS的风险增加，其中一个原因被认为是由于免疫反应受损。我们测试了产前尼古丁暴露损害动态颈动脉化学受体驱动的兴奋性反应的发展，并降低缺氧时降低代谢率的能力的假设。在妊娠第3天将渗透微型泵植入20只妊娠大鼠中，以输送尼古丁（6 mg/kg/天游离碱）或生理盐水4周。在出生后第3、8和18天（n = 6、8和6），记录大鼠幼仔对100%O-2（Dejours试验）和5%O-2 + 5%CO2 5秒挑战的呼吸通气量。颈动脉窦神经（CSN）对缺氧和CO2的反应记录从22个控制和17尼古丁暴露制剂在3-20天之间的年龄。在第3天（尼古丁和对照组各n = 7）和第8天（尼古丁和对照组各n = 5），在室内空气和10% O-2中测量各组幼仔的耗氧量（（V）/点（O2））。尼古丁暴露对CSN反应的发展没有可检测的影响。对5%O-2- 5%CO2的通气反应随年龄增长而增加，但尼古丁组和对照组之间没有差异。在第8天和第18天，对100%O-2的通气反应不受尼古丁暴露的影响。然而，3天的尼古丁组显示没有显着的反应，100%O-2，而VE显着减少，在对照组的100%O-2。尼古丁暴露对缺氧3天或8天时降低耗氧量的能力无显著影响，但在第3天，尼古丁组中耗氧量的基线（室内空气）变异性更大。我们得出结论，尼古丁暴露似乎导致异常的反应，撤回基线外周化学感受器驱动器在一段时间的出生后早期的生活。我们推测，短暂的异常可能会导致一段时间的不稳定，并增加对挑战的脆弱性。(C)1999 Elsevier Science B. V.保留所有权利。
Infants of smoking mothers are at increased risk of SIDS, one cause of which is thought to be due to impaired ventilatory responses. We tested the hypotheses that prenatal nicotine exposure impairs the development of dynamic carotid chemoreceptor-driven ventilatory responses, and reduces the ability to lower metabolic rate in hypoxia. Osmotic minipumps were implanted into 20 pregnant rats at day 3 of gestation to deliver nicotine (6 mg/kg per day free base) or saline for 4 weeks. Minute ventilation was recorded breath by breath in rat pups at 3, 8 and 18 days (n = 6, 8 and 6)postnatal in response to 5-sec challenges of 100% O-2 (Dejours test) and 5% O-2 + 5% CO2. Carotid sinus nerve (CSN) responses to hypoxia and CO2 were recorded from 22 control and 17 nicotine-exposed preparations at ages between 3-20 days. Oxygen consumption ((V)over dot (O2)) was measured in groups of pups at 3 days (n = 7 each for nicotine and control) and 8 days (n = 5 each for nicotine and control) in room air and 10% O-2. There was no detectable effect of nicotine exposure on the development of CSN responses. Ventilatory responses to 5% O-2-5% CO2 increased with age but did not differ between nicotine and control groups. Ventilatory responses to 100% O-2 were unaffected by nicotine exposure at 8 and 18 days. However, the 3-day nicotine group showed no significant response to 100% O-2 whereas VE was significantly reduced in the control group by 100% O-2. There was no significant effect of nicotine exposure on the ability to reduce oxygen consumption in hypoxia at 3 or 8 days, but at 3 days, baseline (room air) variability in oxygen consumption was greater in the nicotine group. We conclude that nicotine exposure appears to result in abnormal ventilatory responses to withdrawal of baseline peripheral chemoreceptor drive during a period of early postnatal life. We speculate that a transient abnormality could contribute to a period of instability and increased vulnerability to challenges. (C) 1999 Elsevier Science B.V. All rights reserved.