Chronic hypoxia enhances the phrenic nerve response to arterial chemoreceptor stimulation in anesthetized rats
Chronic hypoxia enhances the phrenic nerve response to arterial chemoreceptor stimulation in anesthetized rats
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DOI：
10.1152/jappl.1999.87.2.817
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发表时间：
1999-08-01
影响因子：
3.3
通讯作者：
Powell, FL
中科院分区：
文献类型：
--
作者：
Dwinell, MR;Powell, FL
慢性暴露于缺氧会导致通气量随时间增加，称为缺氧通气适应。动脉化学感受器对 Oz 的敏感性增加有助于通气适应缺氧，但也有人假设了其他机制。我们设计这个实验是为了确定中枢神经系统对外周化学感受器输入的处理是否受到慢性缺氧暴露的影响。在记录两组麻醉、通气、迷走神经切断的大鼠的膈神经活动期间，以不同频率（0.5-20 Hz，0.2 毫秒持续时间）对颈动脉窦神经进行超最大刺激。在长期缺氧组（80托激发Po-2 7天）中，膈爆发频率（f（R），爆发/分钟）显着高于颈动脉窦神经刺激频率> 5 Hz的常氧对照组。在长期缺氧组中，综合膈神经活动的峰值幅度（积分 Phr，基线百分比）或积分 Phr 的变化在 5 至 17 Hz 之间的刺激频率下显着更大，并且在刺激频率 > 5 Hz 时分钟膈神经活动（积分 Phr x f(R)）显着更大。这些实验表明，慢性缺氧有助于通过中枢神经系统中的机制将动脉化学感受器传入输入转化为通气传出输出。
Chronic exposure to hypoxia results in a time-dependent increase in ventilation called ventilatory acclimatization to hypoxia. Increased Oz sensitivity of arterial chemoreceptors contributes to ventilatory acclimatization to hypoxia, but other mechanisms have also been hypothesized. We designed this experiment to determine whether central nervous system processing of peripheral chemoreceptor input is affected by chronic hypoxic exposure. The carotid sinus nerve was stimulated supramaximally at different frequencies (0.5-20 Hz, 0.2-ms duration) during recording of phrenic nerve activity in two groups of anesthetized, ventilated, vagotomized rats. In the chronically hypoxic group (7 days at 80 Torr inspired Po-2), phrenic burst frequency (f(R), bursts/min) was significantly higher than in the normoxic control group with carotid sinus nerve stimulation frequencies >5 Hz. In the chronically hypoxic group, peak amplitude of integrated phrenic nerve activity (integral Phr, percent baseline) or change in integral Phr was significantly greater at stimulation frequencies between 5 and 17 Hz, and minute phrenic activity (integral Phr x f(R)) was significantly greater at stimulation frequencies >5 Hz. These experiments show that chronic hypoxia facilitates the translation of arterial chemoreceptor afferent input to ventilatory efferent output through a mechanism in the central nervous system.