Elevated levels of free fatty acids in lung injury associated with acute pancreatitis in rats

Pulmonary injury is associated with acute pancreatitis (AP) in up to 70% of the cases, and may even progress to the adult respiratory distress syndrome (ARDS). Some authors discuss the socalled “free fatty acids” (FFA) to play a certain role in the pathogenesis of AP and in the subsequent systemic complications. We therefore tried to find out what correlations may exist between FFA, pancreatitis, and lung injury in a rat model. AP was induced by infusing 2 different concentrations of glycodeoxycholic acid (GDOC 17 mmol and 34 mmol) into the cannulated pancreatic duct. At set times (2, 6, 12, 24 and 48 hours), the animals were sacrificed, and blood was collected for determining FFA, amylase and pO₂. Pancreas and lungs were removed for histologic examination, and the lung weight was determined. The 2 treatment groups and the control group, which received no infusion after cannulation, were of equal size. GDOC-34 animals developed severe pancreatitis with hemorrhage and necrosis as well as lung injury with edema, inflammatory infiltrates including “foamy macrophages”, hemorrhage, and thickening of the alveolar membrane. In contrast to this, the GDOC-17 animals showed pancreatic edema only until 24 hours, they obviously suffered less severe histologic changes in the lungs. These results together with the corresponding changes in amylase, FFA, pO₂, and lung weight show that AP can be experimentally induced at different levels of severity associated with different degrees of morphologic changes and dysfunctions in the lungs. The clinical course of the disease, the rising amylase levels and lung weights, and the decreasing pO₂ correlate significantly with the FFA values.