Delayed Fluid Resuscitation in Hemorrhagic Shock Induces Proinflammatory Cytokine Response

Chien Chang Lee, I. Jing Chang, Zui Shen Yen, Chiung Yuan Hsu, Shey Ying Chen, Chan Ping Su, Wen Chu Chiang, Shyr Chyr Chen, Wen Jone Chen

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Abstract

Study objective: This study is designed to determine the effects of delayed fluid resuscitation on the hemodynamic changes and cytokine responses in a rat model of hemorrhagic shock. Methods: Wistar male rats (n=40; 8/group) were subjected to a volume-controlled hemorrhagic shock for 30 minutes and received lactated Ringer's solution resuscitation as follows: (1) immediate resuscitation, (2) delayed resuscitation begun 30 minutes after hemorrhage (delayed resuscitation 30), (3) delayed resuscitation begun 45 minutes after hemorrhage (delayed resuscitation 45), (4) delayed resuscitation begun 60 minutes after hemorrhage (delayed resuscitation 60), or (5) unresuscitated group, induction of hemorrhagic shock without resuscitation. Hemodynamic parameters were recorded and blood samples were collected at 0 minutes and at 30, 90, 150, 210, 270, and 330 minutes after hemorrhage for plasma levels of interleukin (IL) 6, IL-10 and tumor necrosis factor α (TNF-α). Repeated-measurement analysis of variance was used for within- and between-groups comparisons. Results: Final mean blood pressure, serum levels of lactate, and hematocrit levels after immediate resuscitation were not different from those in the delayed resuscitation groups. Comparing with the unresuscitated group, TNF-α and IL-6 concentrations were significantly higher, whereas IL-10 concentrations were significantly lower in the 4 resuscitation groups. Circulating concentrations of IL-6 were significantly higher in the delayed resuscitation 45 (P<.001) and delayed resuscitation 60 (P<.001) groups. Circulating concentrations of TNF-α and IL-10 in the 4 resuscitation groups were comparable throughout the experimental period. Conclusion: Delayed fluid resuscitation in hemorrhagic shock induces increased production of proinflammatory cytokines, and the release of cytokine was correlated with the time delayed for resuscitation.

Original languageEnglish
Pages (from-to)37-44
Number of pages8
JournalAnnals of Emergency Medicine
Volume49
Issue number1
DOIs
Publication statusPublished - Jan 1 2007
Externally publishedYes

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Hemorrhagic Shock
Resuscitation
Cytokines
Interleukin-10
Hemorrhage
Interleukin-6
Hemodynamics

ASJC Scopus subject areas

  • Emergency Medicine

Cite this

Delayed Fluid Resuscitation in Hemorrhagic Shock Induces Proinflammatory Cytokine Response. / Lee, Chien Chang; Chang, I. Jing; Yen, Zui Shen; Hsu, Chiung Yuan; Chen, Shey Ying; Su, Chan Ping; Chiang, Wen Chu; Chen, Shyr Chyr; Chen, Wen Jone.

In: Annals of Emergency Medicine, Vol. 49, No. 1, 01.01.2007, p. 37-44.

Research output: Contribution to journalArticle

Lee, Chien Chang ; Chang, I. Jing ; Yen, Zui Shen ; Hsu, Chiung Yuan ; Chen, Shey Ying ; Su, Chan Ping ; Chiang, Wen Chu ; Chen, Shyr Chyr ; Chen, Wen Jone. / Delayed Fluid Resuscitation in Hemorrhagic Shock Induces Proinflammatory Cytokine Response. In: Annals of Emergency Medicine. 2007 ; Vol. 49, No. 1. pp. 37-44.
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abstract = "Study objective: This study is designed to determine the effects of delayed fluid resuscitation on the hemodynamic changes and cytokine responses in a rat model of hemorrhagic shock. Methods: Wistar male rats (n=40; 8/group) were subjected to a volume-controlled hemorrhagic shock for 30 minutes and received lactated Ringer's solution resuscitation as follows: (1) immediate resuscitation, (2) delayed resuscitation begun 30 minutes after hemorrhage (delayed resuscitation 30), (3) delayed resuscitation begun 45 minutes after hemorrhage (delayed resuscitation 45), (4) delayed resuscitation begun 60 minutes after hemorrhage (delayed resuscitation 60), or (5) unresuscitated group, induction of hemorrhagic shock without resuscitation. Hemodynamic parameters were recorded and blood samples were collected at 0 minutes and at 30, 90, 150, 210, 270, and 330 minutes after hemorrhage for plasma levels of interleukin (IL) 6, IL-10 and tumor necrosis factor α (TNF-α). Repeated-measurement analysis of variance was used for within- and between-groups comparisons. Results: Final mean blood pressure, serum levels of lactate, and hematocrit levels after immediate resuscitation were not different from those in the delayed resuscitation groups. Comparing with the unresuscitated group, TNF-α and IL-6 concentrations were significantly higher, whereas IL-10 concentrations were significantly lower in the 4 resuscitation groups. Circulating concentrations of IL-6 were significantly higher in the delayed resuscitation 45 (P<.001) and delayed resuscitation 60 (P<.001) groups. Circulating concentrations of TNF-α and IL-10 in the 4 resuscitation groups were comparable throughout the experimental period. Conclusion: Delayed fluid resuscitation in hemorrhagic shock induces increased production of proinflammatory cytokines, and the release of cytokine was correlated with the time delayed for resuscitation.",
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AU - Chang, I. Jing

AU - Yen, Zui Shen

AU - Hsu, Chiung Yuan

AU - Chen, Shey Ying

AU - Su, Chan Ping

AU - Chiang, Wen Chu

AU - Chen, Shyr Chyr

AU - Chen, Wen Jone

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N2 - Study objective: This study is designed to determine the effects of delayed fluid resuscitation on the hemodynamic changes and cytokine responses in a rat model of hemorrhagic shock. Methods: Wistar male rats (n=40; 8/group) were subjected to a volume-controlled hemorrhagic shock for 30 minutes and received lactated Ringer's solution resuscitation as follows: (1) immediate resuscitation, (2) delayed resuscitation begun 30 minutes after hemorrhage (delayed resuscitation 30), (3) delayed resuscitation begun 45 minutes after hemorrhage (delayed resuscitation 45), (4) delayed resuscitation begun 60 minutes after hemorrhage (delayed resuscitation 60), or (5) unresuscitated group, induction of hemorrhagic shock without resuscitation. Hemodynamic parameters were recorded and blood samples were collected at 0 minutes and at 30, 90, 150, 210, 270, and 330 minutes after hemorrhage for plasma levels of interleukin (IL) 6, IL-10 and tumor necrosis factor α (TNF-α). Repeated-measurement analysis of variance was used for within- and between-groups comparisons. Results: Final mean blood pressure, serum levels of lactate, and hematocrit levels after immediate resuscitation were not different from those in the delayed resuscitation groups. Comparing with the unresuscitated group, TNF-α and IL-6 concentrations were significantly higher, whereas IL-10 concentrations were significantly lower in the 4 resuscitation groups. Circulating concentrations of IL-6 were significantly higher in the delayed resuscitation 45 (P<.001) and delayed resuscitation 60 (P<.001) groups. Circulating concentrations of TNF-α and IL-10 in the 4 resuscitation groups were comparable throughout the experimental period. Conclusion: Delayed fluid resuscitation in hemorrhagic shock induces increased production of proinflammatory cytokines, and the release of cytokine was correlated with the time delayed for resuscitation.

AB - Study objective: This study is designed to determine the effects of delayed fluid resuscitation on the hemodynamic changes and cytokine responses in a rat model of hemorrhagic shock. Methods: Wistar male rats (n=40; 8/group) were subjected to a volume-controlled hemorrhagic shock for 30 minutes and received lactated Ringer's solution resuscitation as follows: (1) immediate resuscitation, (2) delayed resuscitation begun 30 minutes after hemorrhage (delayed resuscitation 30), (3) delayed resuscitation begun 45 minutes after hemorrhage (delayed resuscitation 45), (4) delayed resuscitation begun 60 minutes after hemorrhage (delayed resuscitation 60), or (5) unresuscitated group, induction of hemorrhagic shock without resuscitation. Hemodynamic parameters were recorded and blood samples were collected at 0 minutes and at 30, 90, 150, 210, 270, and 330 minutes after hemorrhage for plasma levels of interleukin (IL) 6, IL-10 and tumor necrosis factor α (TNF-α). Repeated-measurement analysis of variance was used for within- and between-groups comparisons. Results: Final mean blood pressure, serum levels of lactate, and hematocrit levels after immediate resuscitation were not different from those in the delayed resuscitation groups. Comparing with the unresuscitated group, TNF-α and IL-6 concentrations were significantly higher, whereas IL-10 concentrations were significantly lower in the 4 resuscitation groups. Circulating concentrations of IL-6 were significantly higher in the delayed resuscitation 45 (P<.001) and delayed resuscitation 60 (P<.001) groups. Circulating concentrations of TNF-α and IL-10 in the 4 resuscitation groups were comparable throughout the experimental period. Conclusion: Delayed fluid resuscitation in hemorrhagic shock induces increased production of proinflammatory cytokines, and the release of cytokine was correlated with the time delayed for resuscitation.

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