Influence of hypercapnic acidosis and hypoxia on abdominal expiratory nerve activity in the rat
Influence of hypercapnic acidosis and hypoxia on abdominal expiratory nerve activity in the rat
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DOI：
10.1016/j.resp.2007.01.004
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发表时间：
2007-08-01
影响因子：
2.3
通讯作者：
Fregosi, Ralph F.
中科院分区：
文献类型：
--
作者：
Iizuka, Makito;Fregosi, Ralph F.
我们研究了高碳酸性酸中毒和缺氧对麻醉和去脑大鼠腹肌神经驱动的影响；尽管在呼吸生理学和神经生物学中广泛使用大鼠作为实验模型，但这些信息是不可获得的。为了尽量减少肺和胸壁受体的混杂影响，对动物进行迷走神经切除、麻痹和机械通气，并记录腹肌神经的电活动。在麻醉大鼠和去脑大鼠中，两种刺激都引起稳定的低幅度呼气放电，持续整个呼气期（E-all活动），但在吸气期间被抑制。我们还观察到呼气后期，高振幅的爆发（E2活动）叠加在这种稳定的活动上，但仅在呼吸驱动的最高水平。缺氧短暂地增强腹部运动活动，而高碳酸酸中毒则引起活动的持续增加。因此，高碳酸性酸中毒和缺氧都在缺乏相性传入输入的情况下激活腹肌运动神经元。(c) 2007 Elsevier B.V.版权所有
We studied the influence of hypercapnic acidosis and hypoxia on the neural drive to abdominal muscles in anesthetized and decerebrate rats; this information is unavailable despite widespread use of the rat as an experimental model in respiratory physiology and neurobiology. To minimize confounding influences from receptors in the lungs and chest wall, the animals were vagotomized, paralyzed and mechanically ventilated, and electrical activity was recorded from abdominal muscle nerves. In anesthetized and decerebrate rats, both stimuli evoked steady, low amplitude expiratory discharge that persisted throughout the expiratory phase (E-all activity), but was inhibited during inspiration. We also observed late expiratory, high-amplitude bursts (E2 activity) superimposed on this steady activity, but only at the highest levels of respiratory drive. Hypoxia enhanced abdominal motor activity transiently, whereas hypercapnic acidosis caused a sustained increase in activity. Thus, both hypercapnic acidosis and hypoxia activate abdominal muscle motoneurons in the absence of phasic afferent inputs. (c) 2007 Elsevier B.V. All rights reserved.