Bisgard Gerald E, Olson E Burt, Bavis Ryan W, Wenninger Julie, Nordheim Erik V, Mitchell Gordon S
Department of Comparative Biosciences, University of Wisconsin, School of Veterinary Medicine, 2015 Linden Drive, Madison, WI 53706, USA.
Respir Physiol Neurobiol. 2005 Jan 15;145(1):3-11. doi: 10.1016/j.resp.2004.10.008.
Developmental hyperoxia impairs carotid chemoreceptor development and induces long-lasting reduction in carotid sinus nerve (CSN) responses to hypoxia in adult rats. Studies were carried out to determine if CSN responses to acute hypoxia would exhibit hypoxia-induced plasticity in adult 3-5-months-old rats previously treated with postnatal hyperoxia (60% O2, PNH) of 1, 2, or 4 weeks duration. CSN responses to acute hypoxia were assessed in adult rats exposed to 1 week of sustained hypoxia (12% O2, SH). In normal adult rats and adult rats treated with 1 week of PNH, CSN responses to acute hypoxia were significantly increased in urethane-anesthetized rats when studied 3-5 h after SH. Apparent increases in CSN responses to hypoxia were not significant in rats treated with 2 weeks of PNH and were clearly absent after 4 weeks of PNH, but exponential analysis suggests a PNH duration-dependent plasticity of the CSN response to acute hypoxia after SH. In a second study rats exposed to 2 weeks of PNH were treated with SH for 1 week as adults and acute hypoxic responses were tested 4-5 months later. CSN responses in these rats were unaffected by SH suggesting a lack of persistent SH-induced functional plasticity. We conclude that rats treated with 1 week of PNH retain the capacity for hypoxia-induced plasticity of carotid chemoafferent function and some potential for plasticity may be present after 2 weeks of PNH, whereas 4 weeks of PNH impairs the capability of rats to exhibit plasticity following 1 week of SH.
发育性高氧会损害成年大鼠颈动脉化学感受器的发育,并导致成年大鼠颈动脉窦神经(CSN)对低氧的反应长期降低。我们开展了研究,以确定在成年3至5月龄大鼠中,曾接受过持续1、2或4周的出生后高氧(60%氧气,PNH)处理,其CSN对急性低氧的反应是否会表现出低氧诱导的可塑性。对暴露于1周持续低氧(12%氧气,SH)的成年大鼠评估其CSN对急性低氧的反应。在正常成年大鼠和接受1周PNH处理的成年大鼠中,在SH后3至5小时进行研究时,在氨基甲酸乙酯麻醉的大鼠中,CSN对急性低氧的反应显著增加。在接受2周PNH处理的大鼠中,CSN对低氧反应的明显增加并不显著,而在接受4周PNH处理后则明显不存在,但指数分析表明,在SH后,CSN对急性低氧的反应存在PNH持续时间依赖性的可塑性。在第二项研究中,成年后暴露于2周PNH的大鼠作为成年大鼠接受1周的SH处理,并在4至5个月后测试急性低氧反应。这些大鼠的CSN反应不受SH影响,这表明缺乏持续的SH诱导的功能可塑性。我们得出结论,接受1周PNH处理的大鼠保留了颈动脉化学传入功能低氧诱导可塑性的能力,在接受2周PNH处理后可能仍存在一定的可塑性潜力,而接受4周PNH处理会损害大鼠在接受1周SH后表现出可塑性的能力。