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首页> 外文期刊>American Journal of Physiology >Spinal cord injury-induced changes in breathing are not due to supraspinal plasticity in turtles (Pseudemys scripta).
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Spinal cord injury-induced changes in breathing are not due to supraspinal plasticity in turtles (Pseudemys scripta).

机译：脊髓损伤引起的呼吸变化不是由于乌龟的脊髓上可塑性所致（Pseudemys scripta）。

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摘要

After occurrence of spinal cord injury, it is not known whether the respiratory rhythm generator undergoes plasticity to compensate for respiratory insufficiency. To test this hypothesis, respiratory variables were measured in adult semiaquatic turtles using a pneumotachograph attached to a breathing chamber on a water-filled tank. Turtles breathed room air (2 h) before being challenged with two consecutive 2-h bouts of hypercapnia (2 and 6% CO2 or 4 and 8% CO2). Turtles were spinalized at dorsal segments D8-D10 so that only pectoral girdle movement was used for breathing. Measurements were repeated at 4 and 8 wk postinjury. For turtles breathing room air, breathing frequency, tidal volume, and ventilation were not altered by spinalization; single-breath (singlet) frequency increased sevenfold. Spinalized turtles breathing 6-8% CO2 had lower ventilation due to decreased frequency and tidal volume, episodic breathing (breaths/episode) was reduced, and singlet breathing was increased sevenfold. Respiratory variables in sham-operated turtles were unaltered by surgery. Isolated brain stems from control, spinalized, and sham turtles produced similar respiratory motor output and responded the same to increased bath pH. Thus spinalized turtles compensated for pelvic girdle loss while breathing room air but were unable to compensate during hypercapnic challenges. Because isolated brain stems from control and spinalized turtles had similar respiratory motor output and chemosensitivity, breathing changes in spinalized turtles in vivo were probably not due to plasticity within the respiratory rhythm generator. Instead, caudal spinal cord damage probably disrupts spinobulbar pathways that are necessary for normal breathing.
机译：发生脊髓损伤后，尚不清楚呼吸节律发生器是否可塑性补偿呼吸功能不全。为了验证这一假设，使用连接在充满水的水箱上的呼吸室的气压描记器在成年半水龟中测量呼吸变量。乌龟在连续两次持续2小时的高碳酸血症发作（2％和6％的CO2或4％和8％的CO2）之前接受呼吸（2小时）。乌龟在背部D8-D10处脊椎化，因此仅使用胸带运动来呼吸。受伤后第4周和第8周重复测量。对于乌龟来说，呼吸室内空气的呼吸频率，潮气量和通气都不会因脊柱麻痹而改变。单呼吸（单呼吸）频率增加了七倍。呼吸频率为6-8％的海龟由于频率和潮气量减少而通气性降低，间歇性呼吸（呼吸/发作）减少，单峰呼吸增加了7倍。假手术的乌龟的呼吸变量不会因手术而改变。来自对照龟，脊髓龟和假龟的孤立脑干产生相似的呼吸运动输出，并对浴液pH升高做出相同反应。因此，脊柱海龟在呼吸室内空气时可以补偿骨盆带丢失，但在高碳酸血症发作时无法补偿。由于来自对照海龟和脊椎海龟的孤立脑干具有相似的呼吸运动输出和化学敏感性，因此，体内脊椎海龟的呼吸变化可能不是由于呼吸节律产生器内的可塑性引起的。相反，尾脊髓损伤可能会破坏正常呼吸所必需的脊髓球通路。

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