Test object: pathophysiological mechanisms of lung edema. Goal of the study: evaluation of surfactant system condition and hemocirculation in lesser circulation, as well as mechanisms of their disorders in lung edema. Investigation methods: pathophysiological, histological, electron-microscopic, biochemical, pharmacological, physicochemical, and statistical methods. Theoretical and practical value of the obtained results. This study belongs to basic investigations. The experimental data obtained enable broadening and deepening the existing concepts of disorder mechanisms in surfactant system and hemocirculation in lesser circulation in lung edema. The experimental studies performed concerning expediency of using angiotensin converting enzyme (ACE) inhibitors in complex therapy of lung edema present a theoretical basis for further clinical study of a novel adequate pathogenetically justified method of lung edema treatment. Results of the study can be used in following research work, in teaching pathophysiology and other medical sciences, and in clinic for improvement of lung edema treatment. Scientific novelty of the obtained results: the mechanisms of surfactant system disorders in lung edema were revealed for the first time; decrease of reserve surfactant quantity in pneumocyte osmiophilic granules and changes in its phospholipid composition, resulting in morphofunctional disorders of aerohematic barrier, were detected. The role of lung tissue free sulfhydryl groups in lung edema pathogenesis has been studied for the first time. The decrease of free sulfhydryl group content in lung tissue has been found to result in structural and functional changes in lung mitochondrial apparatus and aerohematic barrier, decrease of tissue respiration intensity and respiratory metabolism disorders, which promotes lung edema development. Hemocirculation peculiarities in lung edema, mechanisms of their development, as well as adaptive-compensatory mechanisms were studied in experimental conditions for the first time. We have established that lung edema is accompanied with ultrastructural rearrangements of atrial cardiomyocytes manifested through the decrease in relative volume of cardiomyocyte secretory granules and decrease of atrial natriuretic factor (ANF) content in atria. Increase of ANF blood plasma level in lung edema presents an adaptive-compensatory mechanism promoting hypertension decrease in lesser circulation, directed to normalization of hemodynamic disorders, restoration of lung barrier function and water-electrolytic homeostasis. Expediency of using ACE inhibitors in complex therapy of lung edema has been pathogenetically justified for the first time on the basis of experimental investigation. ACE inhibitors’ application in experimental lung edema has been proven to promote restoration of aerohematic barrier, morphofunctional condition of myocardium, hypertension decrease in lesser circulation, which results in normalization of respiratory pattern and provision of normal respiratory metabolism level, and exerts positive impact on clinical course and treatment efficacy. Implementation degree: the thesis results were implemented in academic activity in the departments of pathological physiology of National Pharmaceutical University, Kharkov; “Ukrainian Medical Dental Academy” HSEU, Poltava; Zaporozhie State Medical University; Donetsk National Medical University; N.I. Pirogov Vinnitsa National Medical University; Bukovina State Medical University, Chernovtsi; Ivano-Frankovsk National Medical University; V.V. Podvysotsky department of general and clinical pathophysiology of Odessa State Medical University.
