Chapters authored
Smoking, Respiratory Diseases and Endothelial Dysfunction
Vascular endothelium actively participates in inflammatory reactions in the majority of chronic respiratory diseases. Smoking is a major risk factor for bronchopulmonary diseases, and it plays an important role in endothelial dysfunction development. Some experiments prove that aggressive pollutants of tobacco smoke (benzopyrene, peroxynitrite, acrolein, cyanides, peroxides, etc.) can cause direct damage to endothelial cells due to expression of adhesion molecules on their surface and intensification of lipid peroxidation. In turn, oxidized lipoproteins in the tunica intima of the vessel work as attractants for chemotaxis of leukocytes and monocytes that start to produce pro-inflammatory cytokines in big amounts. These processes trigger systemic inflammatory response that leads to irreversible thickening of the vessel walls and deterioration of their mechanical properties. Chronic exposure to tobacco smoke and the products of combustion of tobacco leads to chronic system inflammatory reaction, oxidative stress, endothelial dysfunction and morpho-functional damage of target organs. Nowadays, the connection between chronic obstructive pulmonary disease (COPD) and some cardiovascular and cerebrovascular diseases has been well established. Studying the mechanisms of endothelial dysfunction in brain blood vessels of patients with smoking habits and COPD can be very important for preventing acute vascular events.
Part of the book: Endothelial Dysfunction
Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms
This chapter describes endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease (COPD) and smoking on the basis of previously completed studies, literature data, and own researches. As components of neurogenic inflammation in the processes of tissue remodeling in emphysema, we describe the distribution and activity of the substance P, neurokinin-1 and its receptor, tissue metalloproteinases and their tissue inhibitors in the lungs during the entire experimental period, the modeling of COPD in rats with a smoking model. We also analyzed the content of neurokinin system markers, the localization, and markers of tissue metalloproteinases in human lung tissue structures. We have confidence that there is a special morphofunctional continuum of development of lower respiratory tract remodeling in response to chronic exposure to tobacco smoke and the development of inflammation in COPD. New data suggest that imbalance of neuro-mediated interactions, alteration of vasomotoric signaling mechanisms, secretion, mucociliary clearance, cytoprotection involving substance P-dependent components with impaired content, and development of dystopia of matrix metalloproteinases and their tissue inhibitors are involved in the initiation of morphological restructuring. Research in this direction should be continued to allow approaches to the development of preventive and therapeutic strategies for emphysema.
Part of the book: Update in Respiratory Diseases