Background Interleukin-10 (IL-10) counteracts the effects of the proinflamm
atory cytokines interleukin-l (IL-1), interleukin-6 (IL-6), and tumor necro
sis factor (TNF). Experimental data suggest that inhibition of these proinf
lammatory cytokines improves outcome in sepsis, endotoxemia, necrotizing pa
ncreatitis, and other severe inflammatory states. We hypothesized that the
administration of IL-10 would attenuate the release of proinflammatory cyto
kines after severe hemorrhagic shock.
Methods. To test our hypothesis, male Sprague-Dawley rats (N = 20) were div
ided into control and experimental groups. We induced hemorrhagic shock by
removing a sufficient quantity of blood to maintain a mean arterial pressur
e of 50 mm Hg or less for 120 min. The animals were then resuscitated with
shed blood and an equal volume of 0.9% saline. The experimental group recei
ved 10,000 units of IL-10 at the initiation of shock. Serum IL-1, IL-6, TNF
, and lactate were measured at baseline, after 120 min of shock, and 60 min
after resuscitation. The rats were followed for 72 h to calculate survival
.
Results. Similar levels of hypoperfusion were obtained in both groups as de
monstrated by lactate levels and amount of shed blood. The survival rate (7
0%) was the same in both groups. Serum levels of IL-l and IL-6 were not sig
nificantly different between the two groups, although there was a trend tow
ard IL-6 suppression. TNF, however, was significantly lower in the IL-10-tr
eated group at the end of shock (Wilcoxon test, P < 0.025).
Conclusion. Administration of IL-10 suppresses the TNF surge observed after
severe hemorrhagic shock. (C) 2000 Academic Press.