MORPHOFUNCTIONAL STATE OF RESPIRATORY PART OF LUNGS UNDER THE TRYPSIN-INDUCTED PNEUMOPATHIA IN EXPERIMENT
Complex morphofunctional, physico-chemical and biochemical investigation of adaptive mechanisms of respiratory part of lungs was held in condition of short and long-term inﬂuence of trigger trypsin on lungs. Hemodynamic injuries in aerohematic barrier and acute centroacinar emphysema were developed, which manifested into chronic panacinar emphysema under the long action of trypsin. Activation of the lung adaptive mechanisms while the acute experiment were displayed by high level of mechanisms of synthesis, secretion, and catabolism surfactant, and accompanied by increasing surface-active compounds on alveolar surface. The long-term inﬂuence of the factor caused the decrease of surfactant catabolism with its accumulation in lungs then. This anable us to make conclusion that the real culprit of decreasing of surfactant catabolism can be either their exhaustion or phospholipase A 2 inactivation or combination. Accumulation of surface-active compounds on alveolar surface leads to decrease of intraalveolar pressure, that is one of the main reason of development of pulmonary emphysema.