Intravenous contrast medium impairs oxygenation of the pancreas in acute necrotizing pancreatitis in the rat.

OBJECTIVE

Contrast-enhanced computed tomography is widely used to evaluate severe acute necrotizing pancreatitis (ANP) by demonstrating areas of malperfusion, which might indicate irreversible necrosis. Because of our prior finding that the intravenous contrast medium (CM) accentuates the severity of ANP by promoting further necrosis and higher mortality, we sought to investigate the mechanism by which this injury is mediated.

DESIGN

Mild acute pancreatitis was induced in Sprague-Dawley rats with intravenous caerulein hyperstimulation; and severe ANP, with intravenous caerulein plus intraductal glycodeoxycholic acid. Control animals and rats with pancreatitis were randomized to be given intravenous CM or saline.

MAIN OUTCOME MEASURE

Diffuse reflectance spectroscopy was used to measure the index of hemoglobin content and oxygen saturation in pancreatic tissues in vivo.

RESULTS

Oxygen saturation of hemoglobin was increased in animals with mild acute pancreatitis (AP) (mean [+/- SEM], 58.7% +/- 1.2% vs 55.2% +/- 1.5% in control animals; P < .05) and was decreased in animals with ANP (51.2% +/- 1.2% vs 55.2% +/- 1.5%; P < .05). Fifteen minutes after the infusion of CM, oxygen saturation of hemoglobin significantly decreased further in animals with ANP (51.4% +/- 1.8% before infusion of CM vs 46.1% +/- 1.7% at 15 minutes; P < .05) and remained significantly below the comparable group receiving intravenous saline for the entire 60-minute test. This decrement was not observed in animals with ANP given saline or in animals with mild AP or in control animals after infusion of saline or CM. The index of hemoglobin content remained unchanged throughout the experiment in all groups.

CONCLUSIONS

The prolonged reduction of oxygen saturation of hemoglobin in the pancreas following the administration of intravenous CM in rats with severe ANP indicates that CM impairs the pancreatic microcirculation in necrotizing forms of AP. This may explain our previous finding that CM increases pancreatic injury and mortality in rodents with ANP, and it underlines our concern that the use of contrast-enhanced computed tomography early in human AP may promote the evolution of pancreatic necrosis.