Pancreatitis-induced Acute Lung Injury

Abstract

Cerulein-induced acute pancreatitis in rats is associated with acute lung injury characterized by increased pulmonary micro-vascular permeability, increased wet lung weights, and histologie features of alveolar capillary endothelial cell and pulmonary parenchymal injury. The alveolar capillary permeability index is increased 1.8-fold after a 3-hour injury (0.30 to 0.54, p < 0.05). Gravimetric analysis shows a similar 1.5-fold increase in wet lung weights at 3 hours (0.35% vs. 0.51% of total body weight, p < 0.05). Histologie features assessed by quantitative morphometric analysis include significant intra-alveolar hemorrhage (0.57 ± 0.08 vs. 0.12 ± 0.02 RBC/alveolus at 6 hours, p < 0.001); endothelial cell disruption (28.11% vs. 4.3%, p < 0.001); and marked, early neutrophil infiltration (7.45 ± 0.53 vi. 0.83 ± 0.18 PMN/hpf at 3 hours, ñ < 0.001). The cerulein peptide itself, a cholecystokin (CCK) analog, is naturally occurring and is not toxic and in several in vitro settings including exposure to pulmonary artery endothelial cells, Type II epithelial cells, and an ex vivo perfused lung preparation. The occurrence of this ARDS-like acute lung injury with acute pancreatitis provides an excellent experimental model to investigate mechanisms and mediators involved in the pathogenesis of ARDS.