[Endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease]

Emphysema is one of the main manifestations of chronic obstructive pulmonary disease (COPD), and smoking is one of the most significant risk factors. The results of studies in humans and animals show the vascular endothelium initiates and modulates the main pathological processes in COPD and smoking is an important factor initiating, developing and persisting inflammation and remodeling of blood vessels and tissues, including the destruction of small respiratory tracts with the development of lung tissue destruction and emphysema. The latest studies describe mechanisms not just associated with the endothelium, but specific neuro-mediated mechanisms. There is reason to believe that neuro-mediated and neuro-similar mechanisms associated and not related to endothelial dysfunction may play the significant role in the pathogenesis of COPD and emphysema formation. Information about components and mechanisms of neurogenic inflammation in emphysema development is fragmentary and not systematized in the literature. It is described that long-term tobacco smoking can initiate processes not only of cells and tissues damage, but also become a trigger for excessive release of neurotransmitters, which entails whole cascades of adverse reactions that have an effect on emphysema formation. With prolonged and/or intensive stimulation of sensor fibers, excessive release of neuropeptides is accompanied by a number of plastic and destructive processes due to a cascade of pathological reactions of neurogenic inflammation, the main participants of which are classical neuropeptides and their receptors. The most important consequences can be the maintenance and stagnation of chronic inflammation, activation of the mechanisms of destruction and remodeling, inadequate repair processes in response to damage, resulting in irreversible loss of lung tissue. For future research, there is interest to evaluate the possibilities of therapeutic and prophylactic effects on neuro-mediated mechanisms of endothelial dysfunction and damage emphysema in COPD and smoking development.