• Christian Hierholzer, Timothy R Billiar, and David J Tweardy.
• Chirurgische Klinik und Poliklinik, Klinikum rechts der Isar der Technischen Universität München, Germany.
• Arch Orthop Trauma Surg. 2002 Feb 1; 122 (1): 44-7.

AbstractThe activation of nuclear factor (NF)-kappaB contributes to the dysfunctional inflammatory response accompanying resuscitation from hemorrhagic shock (HS), in part through induction of pro-inflammatory cytokines including granulocyte colony-stimulating factor (G-CSF) and interleukin (IL)-6. In previous studies, we demonstrated that G-CSF and IL-6 up-regulation required both the ischemic and resuscitation phases of HS. In this study, we examined whether or not both phases of HS were required for NF-kappaB activation and the kinetics of its activation. Sprague-Dawley rats were subjected to unresuscitated HS with increasing duration of the ischemic phase [compensated HS, 0% shed blood return (SBR); decompensated HS, 35% SBR; and irreversible HS, 70% SBR) or HS (compensated or decompensated)] followed by resuscitation. NF-kappaB activity did not increase in any of the unresuscitated groups compared with sham controls. In contrast, resuscitation as early as 1 h following HS resulted in increased NF-kappaB activity compared with both the unresuscitated shock group and sham controls; NF-kappaB activation persisted for 8 h. Thus, NF-kappaB activation requires both phases of HS, occurs rapidly following resuscitation, and persists throughout the early stages of dysfunctional inflammation following resuscitation.

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