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Background: Proper fluid resuscitation can relieve visceral damage and improve survival in severely burned patients. This study compared the effectiveness of resuscitation with 400mEq/L hypertonic saline (HS) and sodium lactate Ringer's solution (LR) in rats with kidney injury caused by burn trauma.Methods: Rats (Sprague-Dawley) underwent burn injury and were randomized into sham, LR, and HS groups. Samples from the kidney were assayed for water content ratio, histopathology, and oxidative stress (superoxide dismutase (SOD) and malondialdehyde (MDA)). Serum sodium, renal function (creatinine and cystatin (Cys)-C), and inflammatory response (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and high mobility group protein box (HMGB)-1) were also examined as serum markers.Results: Hypertonic saline resuscitation reduced the renal water content ratio and improved renal histopathology caused by severe burns. This effect was accompanied by reductions in serum creatinine and Cys-C as well as TNF-α, IL-1β, and HMGB1. Serum sodium concentration and SOD activity were increased, whereas MDA content was decreased in the kidney tissue of the HS group.Conclusions: The data indicate that 400mEq/L HS solution reduces hyponatremia and renal edema, inhibits the release of inflammatory mediators, and alleviates oxidative stress injury, thus protecting against kidney injury induced by severe burns. [ABSTRACT FROM AUTHOR]

Background An overabundant discharge of inflammatory mediators plays a significant role in intestinal injury throughout the early stages of critical burns. The present study aims to explore the outcome of 200 mM hypertonic saline (HS) resuscitation on the intestinal injury of critically burned rats. Materials and methods Fifty-six Sprague-Dawley rats were randomized into three groups: sham group (group A), burn plus lactated Ringer’s group (group B), and burn plus 200 mM HS group (group C). Samples from the intestine were isolated and assayed for wet-weight-to-dry-weight (W/D) ratio, histopathology analyses, and p38 mitogen-activated protein kinase (MAPK) activity. Serum interleukin 1β (IL-1β) and high mobility group protein box 1 (HMGB1) concentrations were also examined. Results Initial resuscitation with 200 mM Na + HS significantly decreased the intestinal W/D ratio and improved intestinal histopathology caused by severe burn. HS resuscitation also inhibited the increase of serum IL-1β and HMGB1 concentrations, and p38 MAPK activity in the intestine of critically burned rats. Conclusions The overall findings of this study suggest that preliminary resuscitation with 200 mM HS after severe thermal injury reduces intestinal edema, inhibits systemic inflammatory response, and attenuates intestinal p38 MAPK activation, thus reduces burns-induced intestinal injury. [ABSTRACT FROM AUTHOR]

Background: An overabundant discharge of inflammatory mediators plays a significant role in intestinal injury throughout the early stages of critical burns. The present study aims to explore the outcome of 200mM hypertonic saline (HS) resuscitation on the intestinal injury of critically burned rats.Materials and Methods: Fifty-six Sprague-Dawley rats were randomized into three groups: sham group (group A), burn plus lactated Ringer's group (group B), and burn plus 200mM HS group (group C). Samples from the intestine were isolated and assayed for wet-weight-to-dry-weight (W/D) ratio, histopathology analyses, and p38 mitogen-activated protein kinase (MAPK) activity. Serum interleukin 1β (IL-1β) and high mobility group protein box 1 (HMGB1) concentrations were also examined.Results: Initial resuscitation with 200mM Na+ HS significantly decreased the intestinal W/D ratio and improved intestinal histopathology caused by severe burn. HS resuscitation also inhibited the increase of serum IL-1β and HMGB1 concentrations, and p38 MAPK activity in the intestine of critically burned rats.Conclusions: The overall findings of this study suggest that preliminary resuscitation with 200mM HS after severe thermal injury reduces intestinal edema, inhibits systemic inflammatory response, and attenuates intestinal p38 MAPK activation, thus reduces burns-induced intestinal injury. [ABSTRACT FROM AUTHOR]