Non-gas exchange lung functions in experimental alcohol addiction and its combination with traumatic brain injury

Abstract

Aim . To investigate non-gas exchange functions of the lungs in alcohol addiction and its combination with traumatic brain injury (TBI). Materials and methods . Experiments were conducted in 107 adult male rats. In animals of the first group the alcohol addiction was simulated by substitution of water for 20% ethanol solution during 20 weeks. In rats of the second group simulation of alcohol addiction and mild TBI were combined. TBI was modeled by weightdrop of 175 g from 30 cm level method. Intact animals were assumed as reference. Results . Alcohol addiction resulted to a decrease of the total number of alveolar phospholipids with change of their fractional composition that leads to aggravation of lung surface activity; alveolar macrophages absorbing activity was deteriorated and increase of total fluid and lung blood filling was observed in the setting of arterial and venous blood NO level increase. Combination of prolonged ethanol intake and TBI caused to the increase of total surfactant phospholipids; however, low phosphatidylcholine level in its composition promoted increase of lung surface tension. The grade of changes of alveolar macrophages phagocytes activity and lung water balance revealed after ethanol intake was increased in the setting of additional TBI. Conclusion . The obtained results provide evidences of imbalance of lipid and water lung metabolism, lung endothelium dysfunction, decrease of alveolar macrophages activity in alcohol addiction and its combination with TBI.