Journal
ARCHIVES OF ORTHOPAEDIC AND TRAUMA SURGERY
Volume 121, Issue 4, Pages 219-222Publisher
SPRINGER-VERLAG
DOI: 10.1007/s004020000211
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Funding
- NCI NIH HHS [CA 72261] Funding Source: Medline
- NIDDK NIH HHS [R01 DK055664] Funding Source: Medline
- NIGMS NIH HHS [GM 53789] Funding Source: Medline
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Hemorrhagic shock (HS) initiates an inflammatory response that includes increased expression of inducible nitric oxide synthase (iNOS) and production of prostaglandins. Induction of iNOS during the ischemic phase of HS may involve the activation of the hypoxia-inducible factor-1 (HLF-1). Increased expression of cyclooxygenase-2 (COX-2) during HS contributes to prostaglandin production. The aim of this study was to determine whether the ischemic phase of HS results in the activation of HIF-1 and the induction of COX-2. The lungs of rats subjected to I-IS demonstrated a twofold increase in HIF-1 activation (P < 0.01) and a 7.4-fold increase in expression of COX-2 mRNA (P < 0.01) compared with sham controls. The upregulation of iNOS and COX-2 during ischemia are two important early response genes that promote the inflammatory response and may contribute to organ damage through the rapid and exaggerated production of nitric oxide and prostaglandins.
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