SODIUM-TAUROCHOLATE-INDUCED ACUTE NECROTIZING PANCREATITIS DOES NOT AFFECT JEJUNAL OXYGENATION IN PIGS

Objective: To study the influence of experimentally induced acute necr otizing pancreatitis on jejunal oxygen transport, jejunal oxygen consu mption, and mucosal Po-2. Design: Prospective, randomized trial. Setti ng: Animal laboratory. Subjects: Domestic pigs aged 7 to 8 wks. Interv entions: Two groups of pigs were anesthetized with midazolam and sufen tanyl, mechanically ventilated, and hemodynamically monitored. In cont rols (n = 9) and in animals with acute necrotizing pancreatitis (n = 9 ), a segment of the jejunum was isolated and autoperfused in situ. Thr ough an antimesenteric enterotomy, an area of jejunal mucosa was expos ed for mucosal Po-2 measurements. Acute necrotizing pancreatitis was i nduced by the injection of 10 mL of 10% sodium-taurocholate into the m ain pancreatic duct. Both groups received normal saline solution to ke ep pulmonary artery occlusion pressure constant. Measurements: Mucosal Po-2 was assessed with a modified Clark-type multiwire surface electr ode. After two baseline measurements, systemic and regional oxygen tra nsport variables and mucosal Po-2 were determined at designated interv als (20, 40, 60, 100, 120, 160, 200, 240, 280 mins). Main Results: Sys temic hemodynamics and oxygen transport were maintained in both groups . In contrast to controls, all animals with pancreatitis showed gross macroscopic and histologic evidence of severe acute necrotizing pancre atitis at autopsy. There were no significant differences between group s in jejunal blood flow, oxygen transport, oxygen consumption, oxygen extraction ratio, or mucosal Po-2. Conclusions: Our results demonstrat e that, under conditions of sustained systemic hemodynamics, jejunal o xygen transport and mucosal oxygenation are well maintained during the early course of sodium-taurocholate-induced acute necrotizing pancrea titis.