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(Received for publication, November 15, 1996, and in revised form, December 3, 1996)
From the Cardiovascular Biology Laboratory, Endotoxic shock is a life-threatening consequence
of severe Gram-negative infection characterized by vascular smooth
muscle cell relaxation and severe hypotension. The production of nitric oxide (NO), through the inducible NO synthase pathway, has been implicated as a major contributor in this process. We now demonstrate that heme oxygenase (HO), an enzyme that generates carbon monoxide (CO)
in the course of heme metabolism, may also be involved in the
hemodynamic compromise of endotoxic shock. Inducible HO (HO-1) mRNA
levels are dramatically increased in aortic tissue from rats receiving
endotoxin, and this increase in vascular HO-1 message is associated
with an 8.9-fold increase in HO enzyme activity in vivo.
Immunocytochemical staining localizes an increase in HO-1 protein
within smooth muscle cells of both large (aorta) and small (arterioles)
blood vessels. Furthermore, zinc protoporphyrin IX, an inhibitor of HO
activity, abrogates endotoxin-induced hypotension in rats. Studies
performed in rat vascular smooth muscle cells in vitro show
that the induction of HO-1 mRNA is regulated at the level of gene
transcription, and this induction is independent of NO production.
Taken together, these studies suggest that the up-regulation of HO-1,
and the subsequent production of CO, contributes to the reduction in
vascular tone during endotoxic shock.
Volume 272, Number 7,
Issue of February 14, 1997
pp. 4295-4301
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
A LINK TO ENDOTOXIC SHOCK
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