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Objective: to characterize the relationship between the subtype and volume of pulmonary emphysema on the indicators of lung ventilation and gas exchange functions. Material and methods. The data of radiation and functional studies were analyzed in 50 patients. The inclusion criteria were chronic obstructive pulmonary disease and emphysema, which had been diagnosed by computed tomography (CT) and confirmed by two radiologists; comprehensive pulmonary function studies, including spirometry and body plethysmography, were performed; diffusion capacity was measured using a single-breath method, involving inhalation of carbon monoxide, and a breath hold. Patients with primary pulmonary emphysema, any history of pulmonary surgery, and emphysema concurrent with other lung X-ray syndromes (consolidation, cavity) were excluded. CT was performed with a 1-mm thick slice and standard scanning parameters on Toshiba tomographs (Japan). Pulmonary function was tested using a MasterScreen Body Diffusion expert diagnostic unit (VIASYS Healthcare, Germany) in accordance with the criteria for correct pulmonary functional tests proposed by a joint group of experts from the American Thoracic Society and the European Respiratory Society. Volumetric analysis of emphysema was performed using the Lung Volume Analysis software package (Toshiba, Japan). In the study, there was a predominance of male patients (n = 42 (84%)), mainly in the 61-70 age group. Results. The isolated type of emphysema was rare: centrilobular and paraseptal emphysemas were seen in 3 (6%) and 2 (4%) patients, respectively. The mixed type of emphysema was detected in 90% of cases; 33 (66%) patients having a predominant centrilobular component constituted a large proportion. It was determined that as the volume of emphysema increased, the patency of the airways worsened, the static pulmonary volumes increased, the lungs were hyperinflated, pulmonary gas exchange worsened, the bronchial resistance slightly increased during calm breathing. No statistically significant results were found from the point of view of correlations between the volume of emphysema and other parameters of pulmonary function. Conclusion. An increase in the volume of emphysema deteriorates pulmonary function; the greatest contribution to the overall picture is made by the patients with a mixed type of emphysema with a predominance of the centrilobular component.

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.

The paper aimed to present evidence of the effect of some pathophysiological features of chronic obstructive pulmonary disease (COPD) on cardiac remodeling in patients free of overt cardiovascular diseases, traditional cardiovascular risk factors and pulmonary hypertension. Contrary to traditional beliefs that cardiac abnormalities in COPD have been mainly associated with the right ventricle, several recent studies have shown an independent effect of pulmonary hyperinflation and emphysema on left ventricular (LV) diastolic filling and LV hypertrophy. Pulmonary hyperinflation and emphysema cause intrathoracic hypovolemia, low preload, small end-diastolic dimension and mechanical compression of LV chamber which could worsen end-diastolic stiffness. Interestingly, that the presence of LV hypertrophy in COPD patients is important but currently poorly understood area of investigation. Pulmonary hyperinflation, increased arterial stiffness and sympathetic activation may be associated with LV hypertrophy. Two-dimensional ultrasound speckle tracking studies have shown the presence of sub-clinical LV systolic dysfunction in patients even with moderate COPD and free of overt cardiovascular diseases. Sarcopenia related to the inflammatory-catabolic state in COPD and hypoxia could play an important role regarding LV systolic dysfunction. Recent data reported the effects of long-acting bronchodilators on reducing lung hyperinflation (inducing lung deflation). Further studies are required to evaluate the effects of pharmacological lung deflation therapy on cardiac volume and function.

A biopsy of lung tissues was a conventional diagnostic method for detection of disseminated processes in the lung, which weren’t diagnosed on preoperative stage. It was used during surgical anti-relapse treatment of spontaneous pneumothorax (SP). A retrospective analysis of the results of lung parenchyma biopsy was made in 143 patients, who have been operated for SP. Basic entry criteria of the research were: the age younger than 40 years old, a presence of one episode of spontaneous pneumothorax, an absence of complaints for respiratory organs before the development of the first episode of spontaneous pneumothorax. The biopsy with following pathomorphological investigation allowed a formulation of exact variant of disseminated processes, which gave the reason for the development of spontaneous pneumothorax in 9 (6%) patients out of 143. The presence of disseminated processes in the lung was detected with multispiral CT in all these patients on preoperative stage. The study of biopsy material found out the presence of emphysema of different degree of manifestation or fibrosis sites in the rest of the patients. An analysis of presented materials allowed the conclusion, that a performance of biopsy was indicated in the case of suspicion for lung disseminated processes in patients with SP. The biopsy with the following histological study didn’t explain the reason of the development of emphysematous and fibrous changes in lung parenchyma in all other cases. At the same time, it didn’t give the option for pathogenetic treatment and it wasn’t possible to predict the following pathogenesis.

The high resistance of infectious agents to antibiotics that doctors currently face in therapy of acute and chronic diseases, especially in ENT-practice makes it possible for experts to search for alternative paths and to select drugs with a broad spectrum of action. These include colloid silver based drugs with proven microbicidal, virucidal and local protective and anti-inflammatory properties

Objective: to evaluate the efficiency of detection of emphysema in the analysis of lung computed tomography (CT) images using the “Autoplan” program and to compare the data of quantitative analysis and clinical indicators. Material and methods. Sixty patients with chronic obstructive pulmonary disease (COPD) were examined; the diagnosis was confirmed by external respiratory function evaluation; all the patients underwent inspiratory-expiratory CT using a 32-row multidetector CT scanner, followed by postprocessing in the “Autoplan” system. The features of the system were a floating threshold value, constructing a histogram, and the possibility of preserving a report and polygonal models. Echocardiography was performed to evaluate the right heart and to estimate pulmonary arterial pressure. Results. The obtained numerical values of lung density assessment (mean lung density and emphysema index) showed a high efficiency (a sensitivity of as high as 78%, a specificity of as high as 81%) in detecting emphysema. There was evidence for a relationship between the data of quantitative analysis and the values of external respiration function. Analysis of echocardiographic findings revealed that there was a relationship between emphysema index and systolic and diastolic right ventricle wall thickness (Spearman’s rank correlation coefficient from -0.56 to -0.66). Conclusion. Thus, analysis of the lung density CT characteristics provides a physician with objective numerical values, which affect the progression of obstructive changes in patients and the development of signs of chronic cor pulmonale.

The work presents the results of research of a pulmonary tissue of 72 laboratory rats of different ages which within three months have been drinking water with salts of lead, chrome and zinc. By means of anatomical, histological, ultramicroscopic and spectrochemical methods it was established: a concentration of said before ions at the end of experiment was the most increased in lungs of young aged rats – on 126,85%, 104,28% and 34,44% respectively; the most significant morphological changes was noted in lungs of aged experimental rats: it was observed a signs of emphysema transformation (increasing of width of alveolus on 96,0%, width of entrance to alveolus - on 96,0%, width of conducting department - on 7,6%, decreasing of alveolar depth on 16,93%) and the signs of pneumosclerosis (accumulation of connective tissue in lungs and increasing of interstitial space on 11,34%). Noted changes were the result of toxic influence of combination of heavy metal salts on alveolar structures of lungs. This fact affects badly on respiratory function.

The purpose of the work was to determine the consequence of pathomorphological changes of the respiratory part and surfactant system of lungs at hepatic insufficiency, and also to estimate the dynamics of changes of both compensate and decompensate types in experimental model. 88 mature rats both sexes for modeling of the hepatic insufficiency by the Саmегоn’s method were used. Rat lungs were examined in 2, 4, 8 and 16 weeks after beginning of experiment. The increase of the volume of regions with emphysema, dysthelectasis and athelectasis at in the respiratory portion of the lungs were found. The increase of interstitial components with decreasing of relative thickness of epithelial layer of alveoli and the endothelial cells in capillaries were observed in aero-hematic barrier. The increase of vessel permeability, formation of hemorrhages, dysthelectasis and athelectasis are observed in the respiratory portion at chronic hepatic insufficiency. The sclerotic changes in the interalveolar septa with pneumofibrosis are determined in the terminal stages of chronic endotoxicosis.

We summarized the available data on therapeutic, surgical and endoscopic treatment of chronic obstructive pulmonary disease and emphysema that may be used like a bridge to lung transplantation. Treatment of chronic obstructive pulmonary disease and emphysema is expensive. Certain limitations in lung transplantation make to create new methods of treatment of severe emphysema. However, one should be ready for possible complications and carefully select patients for certain treatment to avoid false negative results. Reducing costs or developing cheaper treatments is important for the future and availability of care. The risks and complications associated with surgical treatment of emphysema can make endoscopic surgery preferable for these patients, and this undoubtedly requires further research.

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.