Lung mechanics in experimental pancreatitis

The results of this study in dogs demonstrate an early involvement of the lung in experimental acute pancreatitis, even in the absence of any clinical signs of pulmonary insufficiency. The lungs became edematous as demonstrated by increases in the lung/body and lobe wet/dry weight ratios. These data support the concept that disruption of the alveolar-capillary membrane is the early underlying injury. Surfactant is a phospholipid, a major component of which is lecithin. The release of phospholipase A (or Lecithinase) in the blood by the acutely inflamed pancreas could result in surfactant destruction in the lung with an early drop in the elastic recoil of the lung. The depression of the pressure-volume curves in the animals with acute pancreatitis suggest this concept. The early increase in the lung weight following the onset of the pancreatitis suggests the concept that a capillary leak occurs early and frequently in acute pancreatitis. Although clinically respiratory failure is seen in only 4 to 30 percent of all patients with acute pancreatitis, this study suggests that pulmonary injury may be much more frequent, and that clinical evidence might just be a matter of degree.