Carbon dioxide transport in rats with acute pancreatitis.
CONCLUSIONS
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.


BACKGROUND
Hemodynamic alterations in acute pancreatitis have been described, while little is known about CO2 metabolism.


METHODS
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.


RESULTS
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.
Wang
X
X
Department of Surgery, Lund University Hospital, Sweden.
Andersson
R
R
Kruse
P
P
Ihse
I
I
D000208:Acute Disease; D000818:Animals; D001693:Biological Transport, Active; D001784:Blood Gas Analysis; D002245:Carbon Dioxide / Q000097:blood*; D002756:Cholagogues and Choleretics; D004912:Erythrocytes / Q000378:metabolism; D006454:Hemoglobins / Q000378:metabolism; D008297:Male; D010101:Oxygen Consumption; D010195:Pancreatitis / Q000097:blood* / Q000139:chemically induced; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013656:Taurocholic Acid / Q000633:toxicity
D002756:Cholagogues and Choleretics; D006454:Hemoglobins; D002245:Carbon Dioxide; D013656:Taurocholic Acid