Abstract:

The plateau region, with its unique geographical environment and climatic conditions,has a significant impact on human health. Especially its low oxygen and low air pressure increases the incidence and severity of traumatic brain injury. As the core organ of gas exchange, the function of the lungs is vulnerable to damage in the plateau environment, which in turn exacerbates pulmonary infection after traumatic brain injury and increases mortality rate. This is manifested through pathological changes such as inflammation, edema, and hemorrhage, potentially leading to severe complications such as acute respiratory distress syndrome and neurogenic pulmonary edema. There exists a complex bidirectional functional interaction and information transmission between the brain and lungs. The vagus nerve, as a key neural pathway connecting the brain and the lungs, has an important impact on lung injury by regulating inflammatory responses, vascular permeability and other processes through the cholinergic anti-inflammatory pathway(CAP). Among these, α7 nicotinic acetylcholine receptor (α7nAChR) is a fundamental component of the CAP pathway. The nucleus tractus solitarius (NTS), a key node of the CAP pathway, receives sensory inputs from the lungs via the vagus nerve. The NTS processes and integrates these information, sending signals to other brainstem and forebrain regions to elicit vagal impulses to release acetylcholine delivery to peripheral tissues and organs. This regulate the autonomic nervous system and cardiorespiratory function,exerting anti-inflammatory effects. Therefore, this paper systematically reviews the effects of traumatic brain injury on lung function and the protective role of the cholinergic α7nAChR pathway, providing scientific evidence and strategic insights for the prevention and treatment of plateau impact injuries.

Key words: alpha 7 nicotinic acetylcholine receptor, Brain injuries, Lung injury, Plateau, Blast injury