Wang X, Andersson R, Kruse P, Ihse I
Department of Surgery, Lund University Hospital, Sweden.
Int J Pancreatol. 1996 Apr;19(2):103-12. doi: 10.1007/BF02805223.
The production, release, and transport of carbon dioxide from tissues to blood are facilitated both systemically and in the gastrointestinal tract in acute pancreatitis. Red blood cells are responsible 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 barrier failure in acute pancreatitis.
Hemodynamic alterations in acute pancreatitis have been described, while little is known about CO2 metabolism.
Carbon dioxide metabolism was evaluated by virtual values of venoarterial CO2 concentration differences in the early phase after sham operation or induction of acute pancreatitis by intraductal injection of 5% sodium taurocholate in rats.
In acute pancreatitis, virtual values of the CO2 concentration increased in arterial RBC at 6 and 12 h as well as in caval and portal vein RBC and plasma. Virtual values of the dissolved CO2 concentration were reduced in arterial and portal vein blood. The increment in blood CO2 concentration related to the increase in CO2 tension from arterial 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 oxygen extraction decreased in pancreatitis.
