Activation of STAT proteins in the lung of rats following resuscitation from hemorrhagic shock

C. Hierholzer, J. C. Kalff, T. R. Billiar, D. J. Tweardy*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Hemorrhagic shock (HS) initiates a series of inflammatory processes, including the production of pro-inflammatory cytokines at critical sites such as the lung. We have previously shown that granulocyte colony-stimulating factor (G-CSF) and interleukin-6 (IL-6) mRNA are produced in the lungs of rats subjected to resuscitated HS and that both the ischemic and reperfusion phases of resuscitated HS were required. G-CSF and IL-6 activate STAT (signal transducers and activators of transcription) proteins which may sustain the inflammatory response that follows resuscitation in HS. We tested the hypothesis that STAT proteins are activated in the lungs of rats subjected to re suscitated HS and examined the factors contributing to their activation including duration of shock and duration of resuscitation. Sprague-Dawley rats were subjected to compensated (66.1 ± 1.1 min) or decompensated (157.3 ± 2.3 min) HS (mean arterial pressure 40 mmHg) followed by resuscitation and sacrifice at 4 or 8 h. The amount of activated Stat3 was increased 2.3- to 7-fold compared with sham control animals in all four experimental groups of resuscitated HS. Levels of Stat3 activation increased with increase in duration of shock but did not demonstrate differences at the 4 or 8 h time point of killing. These results indicate that resuscitated HS results in the activation of the intracellular signaling cascade that includes that activation of STAT proteins driven by cytokines such as G-CSF and IL-6.

Original languageEnglish
Pages (from-to)372-375
Number of pages4
JournalArchives of Orthopaedic and Trauma Surgery
Issue number6-7
StatePublished - Jul 1998
Externally publishedYes


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