Kinkead R, Dupenloup L, Valois N, Gulemetova R
Department of Pediatrics, Laval University, Hôpital St-François d'Assise, Unité de Recherche de Périnatalogie, Quebec City, Quebec, Canada G1L 3L5.
J Appl Physiol (1985). 2001 May;90(5):1729-35. doi: 10.1152/jappl.2001.90.5.1729.
To test the hypothesis that stress alters the performance of the respiratory control system, we compared the acute (20 min) responses to moderate hypoxia and hypercapnia of rats previously subjected to immobilization stress (90 min/day) with responses of control animals. Ventilatory measurements were performed on awake rats using whole body plethysmography. Under baseline conditions, there were no differences in minute ventilation between stressed and unstressed groups. Rats previously exposed to immobilization stress had a 45% lower ventilatory response to hypercapnia (inspiratory CO(2) fraction = 0.05) than controls. In contrast, stress exposure had no statistically significant effect on the ventilatory response to hypoxia (inspiratory O(2) fraction = 0.12). Stress-induced attenuation of the hypercapnic response was associated with reduced tidal volume and inspiratory flow increases; the frequency and timing components of the response were not different between groups. We conclude that previous exposure to a stressful condition that does not constitute a direct challenge to respiratory homeostasis can elicit persistent (> or =24 h) functional plasticity in the ventilatory control system.
为了验证应激会改变呼吸控制系统功能这一假设，我们将先前遭受固定应激（每天90分钟）的大鼠对中度低氧和高碳酸血症的急性（20分钟）反应与对照动物的反应进行了比较。使用全身体积描记法对清醒大鼠进行通气测量。在基线条件下，应激组和非应激组之间的分钟通气量没有差异。先前遭受固定应激的大鼠对高碳酸血症（吸入二氧化碳分数=0.05）的通气反应比对照组低45%。相比之下，应激暴露对低氧通气反应（吸入氧气分数=0.12）没有统计学上的显著影响。应激诱导的高碳酸血症反应减弱与潮气量降低和吸气流量增加有关；两组之间反应的频率和时间成分没有差异。我们得出结论，先前暴露于不构成对呼吸稳态直接挑战的应激条件下，可在通气控制系统中引发持续（≥24小时）的功能可塑性。
