Intravenous contrast medium impairs oxygenation of the pancreas in acute necrotizing pancreatitis in the rat
T. Foitzik, D. G. Bassi, C. Fernandez-del Castillo, A. L. Warshaw and D. W. Rattner
Department of Surgery, Massachusetts General Hospital, Boston.
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.
