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Departments of 1 Internal Medicine, 2 Integrative Biology, and 3 Surgery, Trauma Research Center, University of Texas Health Science Center, Houston, Texas 77030
Gastrointestinal stasis during sepsis may be
associated with gastrointestinal smooth muscle dysfunction. Endotoxin
[lipopolysaccharide (LPS)] impairs smooth muscle
contraction, in part through inducible nitric oxide synthase (NOS II)
and enhanced nitric oxide production. We studied the roles of tumor
necrosis factor-
(TNF) and interleukin-1 (IL-1) in this process by
using TNF binding protein (TNFbp) and IL-1 receptor antagonist
(IL-1ra). Rats were treated with TNFbp and IL-1ra, or their vehicles, 1 h before receiving LPS or saline. At 5 h after LPS, contractility was
measured in strips of ileal longitudinal smooth muscle, and NOS II
activity was measured in full-thickness segments of ileum. LPS
decreased maximum stress (mean ± SE) from 508 ± 55 (control) to
355 ± 33 g/cm2
(P < 0.05). Pretreatment with TNFbp
plus IL-1ra prevented the LPS-induced decrease. Separate studies of
TNFbp alone or IL-1ra alone indicated that, at the doses and timing
used, TNFbp was more effective. LPS also increased NOS II activity by
>10-fold (P < 0.01) over control.
This increase was prevented by TNFbp plus IL-1ra
(P = not significant vs. control). We
conclude that the LPS-induced increase in NOS II activity and the
decrease in ileal muscle contractility are mediated by TNF and IL-1.
tumor necrosis factor; interleukin-1; tumor necrosis factor binding protein; interleukin-1 receptor antagonist; soluble tumor necrosis factor receptors; sepsis; nitric oxide; inducible nitric oxide synthase; nitric oxide synthase activity; intestinal transit; endotoxin; ileal smooth muscle
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