The association of type II pneumocytes and endothelial permeability with the pulmonary custocyte system in experimental acute pancreatitis.

BACKGROUND

Pancreatitis-associated pulmonary injury is still associated with substantial mortality, especially when seen as a part of the multiple organ dysfunction syndrome.

METHODS

The present study aimed at evaluating alterations in type II pneumocytes and the potential relationship with the development of pulmonary injury after acute haemorrhagic pancreatitis induced by an intraductal infusion of 5% sodium taurodeoxycholate in the rat.

RESULTS

The results demonstrated that definite alterations in type II pneumocytes were noted 12 and 24 h after induction of pancreatitis, characterized by an increase in the number of vocalized lamellae, the exposed area of type II pneumocytes to alveolar airspace, cellular separation and apoptosis without alterations in cellular membrane integrity. Dysfunction of the pulmonary endothelial barrier was evidenced by an increase in pulmonary albumin flux and the leakage index as well as the migration of lanthanum probes from capillaries to interstitial tissues. The levels of tumour necrosis factor (TNF) in bronchoalveolar lavage fluid significantly increased during the initial phase (3 and 6 h) after pancreatitis. The phagocytic activity of the pulmonary custocyte system increased 3 and 12 h after induction of pancreatitis.

CONCLUSION

Thus, pulmonary endothelial barrier dysfunction, an activated custocyte system, and initial release of TNF seems to be involved in the pathogenesis of pancreatitis-associated type II pneumocyte compromise.