Table 1.
Burn injury alters WBC count, pH, glucose, and BEecf.
Fig 1.
ORS increases urine output and positively alters burn-induced biochemical markers.
Total fluid intake (A) urine output volume (B), and (C) Average glomerular filtration rate (GFR) throughout the duration of the study. Levels of creatinine (D, E) and urea nitrogen in the plasma (F) and the urine (G). Urinary protein (H). Means ± SEM with a different superscript are significantly different (P < 0.05) between treatments for indicated time point and a ᵻ indicates a significant (P < 0.05) difference from the BL value.
Fig 2.
Enteral resuscitation prevents reduction in renal artery diameter.
Computed tomography (CT) scanning (A) was performed pre-injury and immediately prior to euthanasia (termination of experiment 48 h). Renal artery diameter (B), kidney volume (C), weight (D), and wet:dry ratios (E) were quantified. For all parameters measured, changes from baseline to 48 h post burn are represented as mean ± SEM. Groups with different superscripts are significantly different (P < 0.05).
Fig 3.
Renal glycogen content is greatest with fluid deprivation.
(A) Representative H&E staining reveals hallmarks of glomerulonephririts in all groups, to include inflammatory cells (#), clotting with cell debris (*), parietal cell hypertrophy (arrow), and synechia (arrowhead) in all groups. Representation (B) and quantification of the color density reveals significantly higher glycogen content in the fluid deprived group compared with the water and ORS groups (* P < 0.05).
Fig 4.
Fluid deprivation elevates circulating cytokines.
Select circulating cytokines were quantified across all time points (A-E). Average of baseline values of all treatments is set as a reference line and bars represent mean ± SEM. Superoxide dismutase (SOD) activity in the plasma (F) and urinary hemin (G) was quantified at BL, 6, 24, and 48 h and presented as mean ± SEM. Asterisk denotes a significant difference (P < 0.05).