OBJECTIVE: To develop and study an experimental model for severe pancreatitis-associated lung injury. DESIGN: Prospective, randomized, controlled trial. SETTING: University pulmonary laboratory. SUBJECTS: Seventy-eight male Wistar rats. INTERVENTIONS: Pancreatitis was induced by taurocholate injection into the pancreatic duct. Data were compared with data from sham-operated animals. MEASUREMENTS AND MAIN RESULTS: Pulmonary mechanical measurements were performed in anesthetized and mechanically ventilated rats. Alveolar pressure was obtained by the alveolar capsule technique. Lungs were fixed at functional residual capacity by immersion in liquid nitrogen and were submitted to morphometric studies. Dynamic pulmonary elastance was found to be increased in the acute pancreatitis group (2.25 +/- 0.21 vs. 1.62 +/- 0.10 cm H2O/mL [p < .05]). Morphometric signs of distal airway contraction and vasoconstriction were observed. Increased intraalveolar edema rate (55.6 +/- 12.7% vs. 22.6 +/- 9.6% [p < .001]) was detected in the animals with acute pancreatitis. A high degree of pulmonary unevenness and polymorphonuclear infiltration were also detected in the lungs of the acute pancreatitis animals. CONCLUSIONS: In this severe pancreatitis-associated lung injury model, the mechanical and morphologic alterations were similar to those alterations observed in the adult respiratory distress syndrome. This model may prove to be a useful tool to investigate mechanisms and mediators of the respiratory failure induced by acute pancreatitis and other forms of adult respiratory distress syndrome.
OBJECTIVE: To develop and study an experimental model for severe pancreatitis-associated lung injury. DESIGN: Prospective, randomized, controlled trial. SETTING: University pulmonary laboratory. SUBJECTS: Seventy-eight male Wistar rats. INTERVENTIONS:Pancreatitis was induced by taurocholate injection into the pancreatic duct. Data were compared with data from sham-operated animals. MEASUREMENTS AND MAIN RESULTS: Pulmonary mechanical measurements were performed in anesthetized and mechanically ventilated rats. Alveolar pressure was obtained by the alveolar capsule technique. Lungs were fixed at functional residual capacity by immersion in liquid nitrogen and were submitted to morphometric studies. Dynamic pulmonary elastance was found to be increased in the acute pancreatitis group (2.25 +/- 0.21 vs. 1.62 +/- 0.10 cm H2O/mL [p < .05]). Morphometric signs of distal airway contraction and vasoconstriction were observed. Increased intraalveolar edema rate (55.6 +/- 12.7% vs. 22.6 +/- 9.6% [p < .001]) was detected in the animals with acute pancreatitis. A high degree of pulmonary unevenness and polymorphonuclear infiltration were also detected in the lungs of the acute pancreatitis animals. CONCLUSIONS: In this severe pancreatitis-associated lung injury model, the mechanical and morphologic alterations were similar to those alterations observed in the adult respiratory distress syndrome. This model may prove to be a useful tool to investigate mechanisms and mediators of the respiratory failure induced by acute pancreatitis and other forms of adult respiratory distress syndrome.
Authors: J Werner; S C Dragotakes; C Fernandez-del Castillo; J A Rivera; J Ou; D W Rattner; A J Fischman; A L Warshaw Journal: Ann Surg Date: 1998-01 Impact factor: 12.969
Authors: Denis R Morel; Jean-Louis Frossard; Banu Cikirikcioglu; Maxime Tapponnier; Catherine M Pastor Journal: Intensive Care Med Date: 2006-07-15 Impact factor: 17.440