Time course of lung injury in rat acute pancreatitis

Abstract

Objective: Lung injury is a severe complication of acute pancreatitis that increases the mortality rate of the disease. The pathophysiology of acute pancreatitis has been studied in several experimental models, but the kinetics of pulmonary complications in relation to the pancreatic disease is not completely understood. We then studied the severity of acute pancreatitis-associated lung injury over 18 h in rats that had taurocholic acid injection in the pancreatic duct and determined whether blood collected from rats with pancreatitis is toxic enough to induce injury in normal lungs. Design and setting: Prospective, randomized, and controlled animal study in an animal research laboratory in a university hospital. Interventions: We isolated lungs from rats with acute pancreatitis 2, 6, and 18 h after taurocholic acid injection in the biliopancreatic duct and perfused them with blood collected from the same rats. Additionally, blood collected from rats with acute pancreatitis (time-points: 2 and 6 h) was perfused in normal lungs. Measurements and results: Taurocholic acid injection induced a severe pancreatic injury that started as early as 2 h after the injection and persisted without recovery over the 18-h study period. In contrast, the pulmonary injury was transient, appearing at the 6-h time point with recovery by the end of the study. Pulmonary injury was moderate and evidenced mostly during lung reperfusion. Interestingly, blood collected at the 2-h time point in pancreatic rats induced pulmonary injury in normal lungs while blood collected at the 6-h time-point was not toxic. Conclusions: While pancreatic injury persists over the full experimental period, pulmonary injury is transient in our experimental model. The recovery of lung injury by 18 h might be explained by a decrease in the overall toxicity of pancreatic blood over time.

Delayed Production of IL-18 in Lungs and Pancreas of Rats with Acute Pancreatitis

“…Sample collection and lung perfusion were performed 2 h (AP 2h ), 6 h (AP 6h ) or 18 h (AP 18h ) after endotoxin and taurocholic acid administration. To measure lung injury, rat lungs were isolated and perfused at 0 (control), 2, 6 and 18 h after pancreatitis induction, as previously described [11]. Airway pressure, airflow resistance, lung weight changes during perfusion and lung dynamic compliance [tidal volume/(peak airway pressure – positive end-expiratory pressure] were assessed, as previously described [11].…”

“…Anesthetized and ventilated Sprague-Dawley rats were perfused with taurocholic acid (4%; 0.5 ml sodium salts; Sigma) into the pancreatic duct and had instillation of endotoxin from Escherichia coli (3 mg/kg; Sigma) into the trachea [11]. After recovery, the rats were extubated and looked after until sample collection or lung isolation and perfusion.…”

Protective effects and mechanisms of Baicalin and octreotide on renal injury of rats with severe acute pancreatitis

“…Severe acute pancreatitis (SAP) is a fatal systemic disease featuring acute onset, serious conditions, high incidence of complications and 20%-30% of mortality mainly due to multiple organ failure at its early stage [1][2][3][4] . Octreotide has been shown to exert its therapeutic effects on SAP mainly via inhibiting pancreatin secretion, release of inflammatory mediators and platelet aggregation, and reducing endotoxin generation [5][6][7][8] .…”

Time-course proteomic analysis of taurocholate-induced necrotizing acute pancreatitis

“…In the present study, we used proteomic analysis to investigate an experimental model of AP induced by perfusion of taurocholate, a bile acid, into the pancreatic duct [8]. This mechanism of disease induction yields a significantly different phenotype than the cerulein model explored in previously published proteomic studies on AP.…”