Abstract
IntroductionThis study compared the effects of hydroxyethyl starch 130/0.4, hydroxyethyl starch 200/0.5, and succinylated gelatin on oxidative stress and the inflammatory response in a rodent hemorrhagic shock model.MethodsSodium pentobarbital-anesthetized adult male Wistar rats (200 g to 220 g) were subjected to a severe volume-controlled hemorrhage using arterial blood withdrawal (30 mL/kg to 33 mL/kg) and resuscitated with a colloid solution at the same volume as blood withdrawal (hydroxyethyl starch 130/0.4, hydroxyethyl starch 200/0.5, or succinylated gelatin). Arterial blood gas parameters were monitored. Malondialdehyde (MDA) content and myeloperoxidase (MPO) activity in the liver, lungs, intestine, and brain were measured two hours after resuscitation. The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 in the intestine were also measured.ResultsInfusions of hydroxyethyl starch 130/0.4, but not hydroxyethyl starch 200/0.5 or succinylated gelatin, significantly reduced MDA levels and MPO activity in the liver, intestine, lungs and brain, and it also inhibited the production of TNF-α in the intestine two hours after resuscitation. However, no significant difference between hydroxyethyl starch 200/0.5 and succinylated gelatin was observed.ConclusionsHydroxyethyl starch 130/0.4, but not hydroxyethyl starch 200/0.5 or succinylated gelatin, treatment after hemorrhagic shock ameliorated oxidative stress and the inflammatory response in this rat model. No significant differences were observed after hydroxyethyl starch 200/0.5 or succinylated gelatin administration at doses of approximately 33 mL/kg.
Highlights
This study compared the effects of hydroxyethyl starch 130/0.4, hydroxyethyl starch 200/0.5, and succinylated gelatin on oxidative stress and the inflammatory response in a rodent hemorrhagic shock model
No significant differences in pH, partial pressure of carbon dioxide (pCO2), partial pressure of oxygen (pO2) and base excess (BE) values were observed in the groups that underwent hemorrhagic shock at the end of hemorrhage. pH, pCO2, and BE values and hemoglobin content decreased significantly at the end of hemorrhage in hemorrhagic groups, but the pO2 value increased in these groups (P < 0.05 versus baseline)
The present study demonstrated that Hydroxyethyl starch (HES) 130 infusion suppressed oxidative stress and the inflammatory response in a rodent model of controlled hemorrhage compared to HES 200 and GEL
Summary
This study compared the effects of hydroxyethyl starch 130/0.4, hydroxyethyl starch 200/0.5, and succinylated gelatin on oxidative stress and the inflammatory response in a rodent hemorrhagic shock model. Initial survivors of HS are susceptible to the systemic inflammatory response syndrome (SIRS), which triggers multiple organ failure (MOF) and post-traumatic death [3,4,5]. Oxidative stress initiates systemic inflammatory cascades through the enhancement of neutrophil activation [8]. Activated neutrophils release cytotoxic ROS, proteases and elastases which produce tissue injury, an enhanced systemic inflammatory response and MOF [9,10]. Ideal resuscitation strategies should suppress oxidative stress and the systemic inflammatory response after HS in addition to maintaining effective organ perfusion. Direct comparisons of oxidative stress and the inflammatory response after commonly used synthetic colloid infusions in hemorrhagic shock are lacking
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