Yegen Céline-Hivda, Marchant Dominique, Bernaudin Jean-François, Planes Carole, Boncoeur Emilie, Voituron Nicolas
Laboratoire Hypoxie & Poumon, UMR INSERM U1272, Université Sorbonne Paris Nord, Bobigny, France.
Faculté de Médecine, Sorbonne Université, Paris, France.
Front Physiol. 2023 Jun 13;14:1205924. doi: 10.3389/fphys.2023.1205924. eCollection 2023.
Some patients with idiopathic pulmonary fibrosis present impaired ventilatory variables characterised by low forced vital capacity values associated with an increase in respiratory rate and a decrease in tidal volume which could be related to the increased pulmonary stiffness. The lung stiffness observed in pulmonary fibrosis may also have an effect on the functioning of the brainstem respiratory neural network, which could ultimately reinforce or accentuate ventilatory alterations. To this end, we sought to uncover the consequences of pulmonary fibrosis on ventilatory variables and how the modification of pulmonary rigidity could influence the functioning of the respiratory neuronal network. In a mouse model of pulmonary fibrosis obtained by 6 repeated intratracheal instillations of bleomycin (BLM), we first observed an increase in minute ventilation characterised by an increase in respiratory rate and tidal volume, a desaturation and a decrease in lung compliance. The changes in these ventilatory variables were correlated with the severity of the lung injury. The impact of lung fibrosis was also evaluated on the functioning of the medullary areas involved in the elaboration of the central respiratory drive. Thus, BLM-induced pulmonary fibrosis led to a change in the long-term activity of the medullary neuronal respiratory network, especially at the level of the nucleus of the solitary tract, the first central relay of the peripheral afferents, and the Pre-Bötzinger complex, the inspiratory rhythm generator. Our results showed that pulmonary fibrosis induced modifications not only of pulmonary architecture but also of central control of the respiratory neural network.
一些特发性肺纤维化患者存在通气变量受损,其特征为用力肺活量值低,同时呼吸频率增加、潮气量减少,这可能与肺硬度增加有关。肺纤维化中观察到的肺硬度增加也可能对脑干呼吸神经网络的功能产生影响,最终可能会加强或加剧通气改变。为此,我们试图揭示肺纤维化对通气变量的影响,以及肺硬度的改变如何影响呼吸神经元网络的功能。在通过6次重复气管内注入博来霉素(BLM)获得的肺纤维化小鼠模型中,我们首先观察到分钟通气量增加,其特征为呼吸频率和潮气量增加、血氧饱和度降低以及肺顺应性下降。这些通气变量的变化与肺损伤的严重程度相关。我们还评估了肺纤维化对参与中枢呼吸驱动调节的延髓区域功能的影响。因此,BLM诱导的肺纤维化导致延髓神经元呼吸网络的长期活动发生变化,特别是在孤束核水平,它是外周传入神经的第一个中枢中继站,以及前包钦格复合体,即吸气节律发生器。我们的结果表明,肺纤维化不仅会引起肺结构的改变,还会导致呼吸神经网络的中枢控制发生改变。