ABSTRACT
Small concentrations of inhaled anesthetics can induce type II pneumocytes dysfunction and affect surfactant production and exacerbate oxidant mediated lung injury. The aim of the present work was to study the interrelationship between alveolar surfactant lipid composition and that of the lung tissue aiming to understand the sequence of events in the pathogenesis and pathophysiology of acute lung injury [ALI] after inhalation anesthesia. 60 albino rats were used in this study. Lipids were extracted from the lung tissue and alveolar surfactant obtained by bronchoalveolar lavage from rats which were subjected to 1-2% halothane or nitrous oxide anesthetics. The following parameters were determined on the extracted lipids: total lipids [TL], triglycerides [TG], total cholesterol [T-ch], total free fatty acids [FFA], total phospholipids [TPL], phospholipids fractions, lecithin [phosphatidyl cholin Pc], lysolecithin, cephalin [phosphatidyl ethanol amine PI] and sphingomyelin. I- Effect of halothane In the surfactant: Halothane decreased all parameters studied with the exception of FFA and sphingomyelin which was increased compared to controls. Cephalin did not change. However, in the lung FFA, lecithin and lysolecithin increased while all other parameters decreased. II- Effect of nitrous oxide [N[2]O]: In the surfactant: All parameters also decreased except lysolecithin, cephalin and sphingomyelin, which were increased. However, FFA did not change significantly from controls. In the lung: Lecithin, lysolecithin and FFA increased whereas the other parameters decreased. Halothane and N[2]O differ as regards their effect on the lipid profile of the surfactant or lung tissue. The functional significance of the alteration was discussed