L-Arginine-induced acute pancreatitis results in mild lung inflammation without altered respiratory mechanics

• Published in: Experimental lung research 2011-02, Vol.37 (1), p.1-9
• Main Authors: Elder, Alison S. F., Saccone, Gino T. P., Bersten, Andrew D., Dixon, Dani-Louise
• Format: Article
• Language: English
• Subjects: Acute Disease; acute lung injury; Acute Lung Injury - etiology; Acute Lung Injury - immunology; Acute Lung Injury - physiopathology; acute pancreatitis; Amylases - blood; Animals; Arginine; Bronchoalveolar Lavage Fluid - immunology; Disease Models, Animal; inflammation; Inflammation Mediators - blood; Lung - immunology; Lung - physiopathology; Male; Pancreas - immunology; Pancreas - pathology; Pancreatitis - chemically induced; Pancreatitis - complications; Pancreatitis - immunology; Pancreatitis - physiopathology; Peroxidase - metabolism; Pneumonia - etiology; Pneumonia - immunology; Pneumonia - physiopathology; Pulmonary Edema - etiology; Pulmonary Edema - physiopathology; Rats; Rats, Sprague-Dawley; Respiratory Mechanics; Time Factors
• ISSN: 0190-2148; 1521-0499
• DOI: 10.3109/01902148.2010.495822

ABSTRACT Acute lung injury is a common complication of acute pancreatitis (AP) and contributes to the majority of AP-associated deaths. Although some aspects of AP-induced lung inflammation have been demonstrated, investigation of resultant changes in lung function is limited. The aim of this study was to characterize acute lung injury in L-arginine-induced AP. Seven groups of male Sprague-Dawley rats (n = 4-10/group) received 2 intraperitoneal (i.p.) injections of L-arginine (250 mg/100 g) at 6, 12, 24, 36, 48, or 72 hours before measurement of lung impedance mechanics. Control rats (n = 10) received i.p. saline. Bronchoalveolar lavage (BAL), plasma, and pancreatic and lung tissue were collected to determine pancreatic and lung measures of acute inflammation. AP developed between 6 and 36 hours, as indicated by increased pancreatic abnormal acinar cells, myeloperoxidase (MPO) activity, edema, and plasma amylase activity, before beginning to resolve by 72 hours. In the lung, MPO activity increased (2.4-fold) from 12 hours, followed by a modest increase in lung edema at 48 hours, with increased BAL cell count (2.5-fold) up to 72 hours (P < .05). In contrast, no significant changes in lung mechanics were evident over the same period. Despite measurable lung inflammation, no significant deterioration in respiratory function resulted from L-arginine-induced AP.