Ed. Crouser et al., ISCHEMIA REPERFUSION INJURY TO THE ILEUM DOES NOT ACCOUNT FOR THE ILEAL VO(2)-DO(2) ALTERATIONS INDUCED BY ENDOTOXIN/, Journal of critical care, 12(4), 1997, pp. 200-207
Purpose: Endotoxin (lipopolysaccharide [LPS])-induced systemic organ i
njury leads to disruption of normal systemic organ metabolic processes
, which are manifest clinically by signs of accelerated anaerobic meta
bolism leg, tissue acidosis and hyperlactatemia) and altered VO2-DO2 r
elationships. The association of increased anaerobic metabolism with V
O2-DO2 alterations has led to the notion that ischemia/ reperfusion (I
/R) injury may be a prerequisite for the development of VO2-DO2 altera
tions during endotoxemia. However, in contrast to sepsis, in which oxy
gen consumption is often increased, oxygen consumption is severely dec
reased after I/R injury. Based on these observations, we hypothesized
that I/R injury would result in systemic organ VO2-DO2 alterations, wh
ich are distinct from those that occur in sepsis. Materials and Method
s: We used the in situ autoperfused feline ileal preparation to simult
aneously examine microvascular permeability, reflected as the ileal ly
mph to plasma protein concentration ratio (C-L/C-P), and ileal VO2-DO2
relationships after either intravenous LPS (2.0 mg/kg; n = 5) or I/R
injury (n = 5), and in matching controls (n = 5). Results: As expected
, all LPS-treated and I/R-injured animals were found to have extensive
ileal histological damage and marked increases in the C-L/C-P compare
d with controls (0.315 +/- 0.009 and 0.329 +/- 0.034, respectively, v
0.097 +/- 0.009; P < .001, both comparisons). In addition, the critica
l DO2 (DO(2)c) was elevated, and the critical oxygen extraction was de
creased in both the I/R and LPS groups relative to controls. However,
as initially hypothesized, the VO2 at the critical D(O)2 was markedly
decreased in the I/R group compared with that of the LPS group. Conclu
sions: These data indicate that I/R injury is insufficient to account
for the systemic organ VO2-DO2 alterations that occur with LPS injury.
(C) 1997 by W.B. Saunders Company.