Sodium-taurocholate-induced acute necrotizing pancreatitis does not affect jejunal oxygenation in pigs

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To study the influence of experimentally induced acute necrotizing pancreatitis on jejunal oxygen transport, jejunal oxygen consumption, and mucosal Po2.


Prospective, randomized trial.


Animal laboratory.


Domestic pigs aged 7 to 8 wks.


Two groups of pigs were anesthetized with midazolam and sufentanyl, mechanically ventilated, and hemodynamically monitored. In controls (n = 9) and in animals with acute necrotizing pancreatitis (n = 9), a segment of the jejunum was isolated and autoperfusedin situ.Through an antimesenteric enterotomy, an area of jejunal mucosa was exposed for mucosal Po2 measurements. Acute necrotizing pancreatitis was induced by the injection of 10 mL of 10% sodium-taurocholate into the main pancreatic duct. Both groups received normal saline solution to keep pulmonary artery occlusion pressure constant.


Mucosal Po2 was assessed with a modified Clark-type multiwire surface electrode. After two baseline measurements, systemic and regional oxygen transport variables and mucosal Po2 were determined at designated intervals (20, 40, 60, 100, 120, 160, 200, 240, 280 mins).

Main Results:

Systemic 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 pancreatitis at autopsy. There were no significant differences between groups in jejunal blood flow, oxygen transport, oxygen consumption, oxygen extraction ratio, or mucosal Po2.


Our results demonstrate that, under conditions of sustained systemic hemodynamics, jejunal oxygen transport and mucosal oxygenation are well maintained during the early course of sodium-taurocholate-induced acute necrotizing pancreatitis. (Crit Care Med 1994; 22:135-141)

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