[Experimental study on the pathogenesis of pulmonary insufficiency in acute pancreatitis and changes in the pulmonary surfactant].

Serious pulmonary complications are often associated with acute pancreatitis. The destruction of pulmonary surfactant by the action of pancreatic phospholipase A2 (PLA2), together with pulmonary edema, is considered an important etiopathogenic factor of acute respiratory insufficiency. This experimental study was undertaken to elucidate the destruction of pulmonary surfactant in acute pancreatitis using the lung pressure volume curve (P-V curve). Acute hemorrhagic pancreatitis was induced in mongrel dogs by a retrograde injection of Na-taurocholate into the main pancreatic duct. Pulmonary surface tension was measured by P-V curve and the effect of PLA2 on pulmonary surfactant was assessed by the ratio of lysolecithin and lecithin, which are essential components of pulmonary surfactant (Ly/Le) in lung wash. Extravascular lung water volume (Ww/Dw) and blood gases were also measured. The value of Ly/Le and serum PLA2 rose significantly from the 3rd hour. On the contrary, no significant differences were seen on P-V curve until the 12th hour but after 20 hours surface tension increased significantly. Ww/Dw and A-aDO2 increased after 3 and 12 hours, respectively. These findings, the degradation of lecithin and the elevation of surface tension accompanied with an increase of serum PLA2, suggest that pulmonary surfactant is destroyed in severe acute pancreatitis, and that the increased capillary permeability of the lung precedes the deterioration of surface tension as the cause of pulmonary insufficiency.