Conclusion: The production, release, and transport of carbon dioxide f
rom tissues to blood are facilitated both systemically and in the gast
rointestinal tract in acute pancreatitis, Red blood cells are responsi
ble for the major exchange and transport of this increase in CO2. The
existence of arteriovenous shunting within the intestine is associated
with tissue ischemia, which may be involved in the etiology of gut ba
rrier failure in acute pancreatitis. Background: Hemodynamic alteratio
ns in acute pancreatitis have been described, while little is known ab
out CO2 metabolism. Methods: Carbon dioxide metabolism was evaluated b
y virtual values of venoarterial CO2 concentration differences in the
early phase after sham operation or induction of acute pancreatitis by
retrograde intraductal injection of 5% sodium taurocholate in rats. R
esults: In acute pancreatitis, virtual values of the CO2 concentration
increased in arterial RBC at 6 and 12 h as well as in caval and porta
l vein RBC and plasma. Virtual values of the dissolved CO2 concentrati
on were reduced in arterial and portal vein blood. The increment in bl
ood CO2 concentration related to the increase in CO2 tension from arte
rial to caval or portal vein valves at constant CO2 tension, The total
increment in CO2 concentration from arterial to caval or portal vein
blood increased. Whole body oxygen extraction increased, whereas gut o
xygen extraction decreased in pancreatitis.