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Pancreatitis-induced acute lung injury. An ARDS model. Ann Surg 1988 Jul;208(1):71-7



Pubmed ID


Pubmed Central ID




Scopus ID

2-s2.0-0023919675   80 Citations


Cerulein-induced acute pancreatitis in rats is associated with acute lung injury characterized by increased pulmonary microvascular permeability, increased wet lung weights, and histologic 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 less than 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 less than 0.05). Histologic 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 less than 0.001); endothelial cell disruption (28.11% vs. 4.3%, p less than 0.001); and marked, early neutrophil infiltration (7.45 +/- 0.53 vs. 0.83 +/- 0.18 PMN/hpf at 3 hours, p less than 0.001). The cerulein peptide itself, a cholecystokinin (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.

Author List

Guice KS, Oldham KT, Johnson KJ, Kunkel RG, Morganroth ML, Ward PA


Keith T. Oldham MD Professor in the Surgery department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Capillary Permeability
Disease Models, Animal
Infusions, Intravenous
Iodine Radioisotopes
Organ Size
Rats, Inbred Strains
Respiratory Distress Syndrome, Adult
jenkins-FCD Prod-387 b0ced2662056320369de4e5cd5f21c218c03feb3