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J. Exp. Med.,
Volume 187, Number 6, March 16, 1998 917-928
By
§
From the * Department of Surgery, the Resuscitation from hemorrhagic shock induces profound changes in the physiologic processes
of many tissues and activates inflammatory cascades that include the activation of stress transcriptional factors and upregulation of cytokine synthesis. This process is accompanied by acute
organ damage (e.g., lungs and liver). We have previously demonstrated that the inducible nitric
oxide synthase (iNOS) is expressed during hemorrhagic shock. We postulated that nitric oxide
production from iNOS would participate in proinflammatory signaling. Using the iNOS inhibitor N6-(iminoethyl)-L-lysine or iNOS knockout mice we found that the activation of the
transcriptional factors nuclear factor Department of Medicine, the § Department of Molecular
Genetics and Biochemistry, and the University of Pittsburgh Cancer Institute, University of
Pittsburgh, Pittsburgh, Pennsylvania 15213; and the ** Beatrice & Samuel A. Seaver Laboratory,
Department of Medicine, Cornell University Medical College, New York 10021
B and signal transducer and activator of transcription 3 and increases in IL-6 and G-CSF messenger RNA levels in the lungs and livers measured 4 h
after resuscitation from hemorrhagic shock were iNOS dependent. Furthermore, iNOS inhibition resulted in a marked reduction of lung and liver injury produced by hemorrhagic shock.
Thus, induced nitric oxide is essential for the upregulation of the inflammatory response in resuscitated hemorrhagic shock and participates in end organ damage under these conditions.
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