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London Health Sciences Centre Research Incorporated and the Departments of Medical Biophysics and Surgery, University of Western Ontario, London, Ontario, Canada N6A 4G5
A normotensive model of hindlimb
ischemia-reperfusion in Wistar rats was used to test the
hypothesis that microvascular perfusion deficits contribute to the
initiation of remote hepatic injury during a systemic inflammatory
response. Animals were randomly assigned to one of three groups: 4 h of
ischemia with 6 h of reperfusion (I/R-6;
n = 4), 4 h of ischemia with 3 h of reperfusion (I/R-3; n = 5), or no
ischemia (naive; n = 5). With
intravital fluorescence microscopy, propidium iodide (PI; 0.05 mg/100 g
body wt) was injected for the in vivo labeling of lethally injured
hepatocytes
(number/10
1
mm3). PI-positive hepatocytes
increased progressively over the 6-h period (naive 32.9 ± 7.8 vs.
I/R-3 92.8 ± 11.5 vs. I/R-6 232 ± 39.2), with no difference between
periportal and pericentral regions of the lobule. Additionally, a
significant decrease in continuously perfused sinusoids (naive 70.0 ± 1.5 vs. I/R-3 65.0 ± 1.0 vs. I/R-6 48.8 ± 0.9%) was
measured. Regional sinusoidal perfusion differences were only observed
after 3 h of limb reperfusion. Indirect measures of hepatocellular
injury using alanine transaminase levels support the progressive nature
of hepatic parenchymal injury (0 h 57.8 ± 6.5 vs. 3 h 115.3 ± 20.7 vs. 6 h 125.6 ± 19.5 U/l). Evidence from this study suggests
that remote hepatic parenchymal injury occurs early and progresses
after the induction of a systemic inflammatory response and that
microvascular perfusion deficits are not essential for the initiation
of such injury.
intravital microscopy; ischemia-reperfusion; remote injury; microcirculation
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