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0371. Temporal changes in systemic and renal inflammation and histology in a 72-hour rat model of faecal peritonitis
© Arulkumaran et al; licensee Springer. 2014
Published: 26 September 2014
Mechanisms underlying sepsis-induced acute kidney injury remain uncertain with inflammation and altered haemodynamics being implicated.
To determine temporal changes in systemic and renal inflammation, and histology, in a 72 hour fluid-resuscitated model of sepsis.
Tunnelled central venous (for fluid administration) and arterial (for BP monitoring/blood sampling) lines were inserted into male Wistar rats under isoflurane anaesthesia. Sepsis was induced 24h later by i.p. injection of faecal slurry. Fluid resuscitation was commenced at 2h post-slurry. Cardiac output was assessed by echocardiography. Animals (n=6-8 per group) were sacrificed at 6, 12, 24, 48, or 72h with kidneys taken for histological section and cytokine (IL-1β, IL-10 by ELISA) analysis, and blood samples for renal biochemistry, and pro- (IL-1β, IL-6), and anti-inflammatory cytokine (IL-10) analysis by ELISA. Renal histology was assessed by light microscopy for features of tubular injury (dilated tubules, tubular casts, cell necrosis), and cell death using TUNEL stain. Comparison was made against sham-operated controls and naïve animals. Statistics were performed using ANOVA and post-hoc Tukey's test. Values are expressed as means±standard deviation.
Serum IL-1β (pg/mL)
Renal IL-1β (pg/µg protein)
Renal IL-10 (pg/µg protein)
Temporal changes in renal inflammation and dysfunction lag behind changes in systemic inflammation and cardiac dysfunction. Renal dysfunction, as measured by serum creatinine, corresponds to renal inflammation. Cell death does is not a predominant feature, and does not account for the renal dysfunction seen in this sepsis model.
NA is supported by the Wellcome Trust
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.