Environmental hyperoxia and development of carotid chemoafferent function.
Environmental hyperoxia and development of carotid chemoafferent function.
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环境高氧和颈动脉化学传入功能的发展。
DOI：
10.1007/978-0-387-73693-8_5
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发表时间：
2008
影响因子：
--
通讯作者：
OlsonJr,EBurt
中科院分区：
文献类型：
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作者：
Bisgard,Gerald;Wenninger,Julie;Wang,Zunyi;OlsonJr,EBurt
生命最初几周暴露于高氧环境会导致大鼠颈动脉化学感受器功能终生受损，例如颈动脉窦神经（CSN）和膈神经对急性缺氧的反应减弱。我们确定了麻醉成年大鼠在出生后高氧（60% O2）1、2 和 4 周（PNH）后对严重缺氧（100% N2 通气）或窒息（停止呼吸机）的最大 CSN 反应。与对缺氧刺激的急性反应一样，我们发现最大 CSN 反应显着减弱，减弱的严重程度取决于 PNH 的持续时间。我们认为，PNH 产生的颈动脉化学传入输入受损可能在婴儿和成人严重缺氧状态下的唤醒失败中发挥作用。
Exposure to hyperoxia in the first few weeks of life causes life-long impairment of carotid chemoreceptor function in rats,e.g., depressed carotid sinus nerve (CSN) and phrenic nerve responses to acute hypoxia. We determined the maximal CSN responses of anesthetized adult rats to severe hypoxia (ventilation with 100% N2) or asphyxia (stopped ventilator) after 1, 2, and 4 weeks of postnatal hyperoxia (60% O2) (PNH). As with acute responses to hypoxic stimuli, we find that maximal CSN responses are significantly attenuated with severity of attenuation dependent on duration of PNH. We suggest that impaired carotid chemoafferent input produced by PNH could play a role in failure of arousal in severely hypoxic states occurring in infants and adults.