To compare acute pulmonary changes secondary to sodium taurocholate hemorrhagic pancreatitis with those changes secondary to a less severe pancreatitis induced by saline infusion into the biliopancreatic duct.
Prospective, randomized controlled trial.
University pulmonary laboratory.
A total of 110 male Wistar rats.
Pancreatitis was induced by either 0.5 mL of a 4% solution of sodium taurocholate (TAU group) or 0.5 mL of normal saline (SAL group) injection into the biliopancreatic duct. Data were compared with data from control (sham-operated) animals (SHAM group).
The severity of pancreatic and pulmonary injuries was evaluated 1, 3, and 8 days after the induction of acute pancreatitis by morphometric and pulmonary mechanical studies. Biliopancreatic duct pressure was measured during infusion of solutions in SAL and TAU groups. SAL and TAU groups developed an intense necrohemorrhagic pancreatitis on day 1 without differences in biliopancreatic duct pressures (134.0 ± 45.1 cm H2O vs. 123.3 ± 23.4 cm H2O). Acute pancreatic lesions were still intense on day 3 in the TAU group only. Pulmonary resistance in SAL and TAU groups was significantly greater than in the SHAM group on day 3 only. On day 1, there was an increase in intraalveolar edema in both groups (p < .02). There was an increase in polymorphonuclear cells in alveolar septa on day 1 only in the TAU group (p < .001). In contrast, both experimental groups presented greater values of PMN cells on day 8 compared with the SHAM group (p < .001). Both groups with pancreatitis showed an increase in alveolar distention and collapse on day 1 that persisted only in the TAU group on days 3 and 8. No deaths were observed in the control (SHAM) group. In contrast, the SAL group had lower mortality than the TAU group in the first two days (17% and 52%, respectively, p = .03).
High-pressure infusion of normal saline into the biliopancreatic duct of rats results in significant pancreatic and lung alterations. These changes are worse in the presence of sodium taurocholate.
From the Departments of Medicine (Drs. Lichtenstein, Milani Jr., Leme, and Martins) and Pathology (Drs. Fernezlian and Capelozzi), Faculty of Medicine, University of Sao Paulo, Brazil.
Supported, in part, by the following Brazilian Scientific Agencies: Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq); Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) and Programa de Núcleos de Excelência (PRONEX-MCT).
Address requests for reprints to: Milton A. Martins, MD, Departamento de Clínica Médica, Faculdade de Medicina da Universidade de São Paulo, Av. Dr. Arnaldo 455 sala 1216, São Paulo - SP - 01246-903, Brazil. E-mail: email@example.com