Abstract：
Exposure to acute intermittent hypoxia (AIH) elicits a form of respiratory plasticity known as long-term facilitation (LTF). Interest has grown in developing AIH interventions to treat ventilatory insufficiency, with promising results in spinal cord injury and amyotrophic lateral sclerosis. Therapeutic AIH may have application in neuromuscular disorders including muscular dystrophies. We sought to establish hypoxic ventilatory responsiveness and the expression of ventilatory LTF in X-linked muscular dystrophy (mdx) mice.Experiments were performed in 15 male wild-type (BL10) and 15 male mdx mice at 4 months of age. Ventilation was assessed using whole-body plethysmography. Baseline measures of ventilation and metabolism were established. Mice were exposed to 10 successive bouts of hypoxia, each lasting 5 min, interspersed with 5-min bouts of normoxia. Measurements were taken for 60 min following termination of AIH.In mdx mice, ventilation was significantly increased 60 min post-AIH compared to baseline. However, metabolic CO2 production was also increased. Therefore, ventilatory equivalent was unaffected by AIH exposure, i.e., no ventilatory LTF manifestation. In wild-type mice, ventilation and metabolism were not affected by AIH.Eliciting ventilatory LTF is dependent on many factors and may require concomitant isocapnia or hypercapnia during AIH exposures and/or repeated daily AIH exposures, which is worthy of further pursuit.
摘要：
暴露于急性间歇性缺氧（AIH）会引起一种称为长期促进（LTF）的呼吸可塑性。人们对开发AIH干预措施以治疗通气功能不全的兴趣越来越大，在脊髓损伤和肌萎缩侧索硬化症中取得了有希望的结果。治疗性AIH可在包括肌营养不良的神经肌肉病症中具有应用。我们试图在X连锁肌营养不良（mdx）小鼠中建立低氧通气反应性和通气性LTF的表达。在15只4月龄的雄性野生型(BL10)小鼠和15只雄性mdx小鼠中进行实验。使用全身体积描记术评估通气。建立通气和代谢的基线测量。小鼠连续10次缺氧,每次持续5分钟，散布着5分钟的常氧发作。在AIH终止后进行60分钟的测量。在mdx小鼠中，与基线相比,AIH后60分钟通气量显著增加.然而,代谢二氧化碳的产生也增加。因此,通气当量不受AIH暴露的影响，即，无通气LTF表现。在野生型小鼠中,通气和代谢不受AIH的影响。诱发通气LTF取决于许多因素，在AIH暴露和/或重复的每日AIH暴露期间可能需要伴随等碳酸血症或高碳酸血症。这是值得进一步追求的。
