Carbon dioxide (CO₂), a primary product of oxidative metabolism, can be sensed by eukaryotic cells eliciting unique responses via specific signalling pathways. Severe lung diseases such as chronic obstructive pulmonary disease are associated with hypoventilation that can lead to the elevation of CO₂ levels in lung tissues and the bloodstream (hypercapnia). However, the pathophysiological effects of hypercapnia on the lungs and specific lung cells are incompletely understood. We have recently reported using combined unbiased molecular approaches with studies in mice and cell culture systems on the mechanisms by which hypercapnia alters airway smooth muscle contractility. In this review, we provide a pathophysiological and mechanistic perspective on the effects of hypercapnia on the lung airways and discuss the recent understanding of high CO₂ modulation of the airway contractility.

二氧化碳 (CO ₂ ) 是氧化代谢的主要产物，可以被真核细胞感知，通过特定的信号通路引发独特的反应。严重的肺部疾病如慢性阻塞性肺病与通气不足有关，可导致 CO ₂升高肺组织和血液中的水平（高碳酸血症）。然而，高碳酸血症对肺和特定肺细胞的病理生理影响尚不完全清楚。我们最近报道了使用联合无偏分子方法对小鼠和细胞培养系统进行研究，研究高碳酸血症改变气道平滑肌收缩力的机制。在这篇综述中，我们提供了关于高碳酸血症对肺气道影响的病理生理学和机械学观点，并讨论了最近对高 CO ₂调节气道收缩力的理解。