Resuscitation with hydroxyethyl starch solution prevents nuclear factor κB activation and oxidative stress after hemorrhagic shock and resuscitation in rats

Ming Che Tsai, Wei Ju Chen, Cheng Hsin Ching, Jih-Ing Chuang

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Fluid resuscitation is vital for treating traumatic hemorrhagic shock (HS), but reperfusion is believed to have the adverse consequences of generating reactive oxygen species and inflammatory cytokines, both of which cause multiple organ dysfunctions. We investigated the effects of various resuscitation fluids on the changes of redox-sensitive molecules after HS and fluid resuscitation (HS/R). We induced HS by bleeding male Sprague-Dawley rats to a blood pressure of 30 to 40 mmHg for 60 minutes. Thirty minutes later, the rats were killed (HS group) or immediately resuscitated with shed blood (HS + BL group), l-isomer lactated Ringer's solution (HS + LR group), or hydroxyethyl starch (HS + HES group). After HS, we found a significant increase in nuclear factor κB DNA binding activity, which was effectively inhibited using HES solution or blood resuscitation. Moreover, resuscitation with blood or LR solution, but not HES solution, induced significant oxidative stress, manifested by a high ratio of oxidized glutathione to reduced glutathione in the lungs, liver, and spleen. HS alone, however, did not increase the ratio of the oxidized glutathione to reduced glutathione in all organs. Although the protein expression of anti-apoptotic Bcl-2 and pro-apoptotic Bax varied in different organs, we found that resuscitation using HES solution prevented the HS-induced reduction of the Bcl-2/Bax ratio in the heart. HES solution was an appropriate resuscitation fluid in reversing nuclear factor κB activation, maintaining the Bcl-2/Bax ratio, and preventing oxidative stress after acute HS.

Original languageEnglish
Pages (from-to)527-533
Number of pages7
JournalShock
Volume27
Issue number5
DOIs
Publication statusPublished - 2007 May 1

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Hemorrhagic Shock
Resuscitation
Starch
Oxidative Stress
Glutathione Disulfide
Glutathione
Traumatic Shock
Apoptosis Regulatory Proteins
Reperfusion
Oxidation-Reduction
Sprague Dawley Rats
Reactive Oxygen Species
Spleen

All Science Journal Classification (ASJC) codes

  • Critical Care and Intensive Care Medicine
  • Physiology

Cite this

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abstract = "Fluid resuscitation is vital for treating traumatic hemorrhagic shock (HS), but reperfusion is believed to have the adverse consequences of generating reactive oxygen species and inflammatory cytokines, both of which cause multiple organ dysfunctions. We investigated the effects of various resuscitation fluids on the changes of redox-sensitive molecules after HS and fluid resuscitation (HS/R). We induced HS by bleeding male Sprague-Dawley rats to a blood pressure of 30 to 40 mmHg for 60 minutes. Thirty minutes later, the rats were killed (HS group) or immediately resuscitated with shed blood (HS + BL group), l-isomer lactated Ringer's solution (HS + LR group), or hydroxyethyl starch (HS + HES group). After HS, we found a significant increase in nuclear factor κB DNA binding activity, which was effectively inhibited using HES solution or blood resuscitation. Moreover, resuscitation with blood or LR solution, but not HES solution, induced significant oxidative stress, manifested by a high ratio of oxidized glutathione to reduced glutathione in the lungs, liver, and spleen. HS alone, however, did not increase the ratio of the oxidized glutathione to reduced glutathione in all organs. Although the protein expression of anti-apoptotic Bcl-2 and pro-apoptotic Bax varied in different organs, we found that resuscitation using HES solution prevented the HS-induced reduction of the Bcl-2/Bax ratio in the heart. HES solution was an appropriate resuscitation fluid in reversing nuclear factor κB activation, maintaining the Bcl-2/Bax ratio, and preventing oxidative stress after acute HS.",
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Resuscitation with hydroxyethyl starch solution prevents nuclear factor κB activation and oxidative stress after hemorrhagic shock and resuscitation in rats. / Tsai, Ming Che; Chen, Wei Ju; Ching, Cheng Hsin; Chuang, Jih-Ing.

In: Shock, Vol. 27, No. 5, 01.05.2007, p. 527-533.

Research output: Contribution to journalArticle

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