Interleukin-1beta alters the oxygen delivery-oxygen consumption relationship in rabbits by increasing the slope of the supply-independent line.
When systemic oxygen delivery (DO2) is reduced, oxygen consumption (VO2) is maintained until a critical level is reached (DO2crit). Sepsis is thought to shift DO2crit to the right and lengthen the supply-dependent portion. We tested the effect of interleukin (IL)-1beta, which is one of the key cytokines related to sepsis, on the DO2-VO2 relationship. Fifteen rabbits were subjected to stepwise cardiac tamponade to reduce DO2 to 10% by inflating a handmade balloon placed into the pericardial sac. Seven rabbits were given 10 microg/kg of IL-1beta intravenously (IL-1beta group) prior to the graded cardiac tamponade. The remainder received saline alone (control group). The DO2-VO2 relationship was analyzed by the dual-line method. IL-1beta significantly decreased mean arterial pressure (65 +/- 11 mmHg from baseline 85 +/- 7 mmHg) without altering cardiac output. The IL-1beta group showed significantly steeper supply-independent line slopes than did the control group (0.19 +/- 0.02 vs. 0.11 +/- 0.02, respectively), which resulted in a DO2crit shift to the left (IL-1beta group, 8.7 +/- 1.7 ml/kg x min vs. control, 11.7 +/- 0.7 ml/kg x min). The IL-1beta group also showed greater PO2 and plasma lactate levels in the portal vein than did the control group. These results indicate that IL-1beta impairs systemic oxygen uptake even before VO2 becomes supply-dependent, presumably due to maldistribution of the blood flow including the splanchnic circulation.
Kuwagata
Y
Y
Department of Acute Critical Medicine, Osaka University Medical School, Suita, Japan.
Oda
J
J
Matsuyama
S
S
Nishino
M
M
Hashiguchi
N
N
Ogura
H
H
Tanaka
H
H
Sugimoto
H
H
D000818:Animals; D002305:Cardiac Tamponade / Q000150:complications / Q000378:metabolism*; D005260:Female; D006801:Humans; D007022:Hypotension / Q000139:chemically induced; D000860:Hypoxia / Q000378:metabolism*; D007375:Interleukin-1 / Q000494:pharmacology* / Q000633:toxicity; D019344:Lactic Acid / Q000097:blood; D023421:Models, Animal; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption / Q000187:drug effects*; D011169:Portal Vein; D011817:Rabbits; D011994:Recombinant Proteins / Q000494:pharmacology; D012769:Shock / Q000209:etiology / Q000378:metabolism*; D013152:Splanchnic Circulation
D007375:Interleukin-1; D011994:Recombinant Proteins; D019344:Lactic Acid; D010100:Oxygen