Hemorrhagic Shock
Vital organ injury and dysfunction in hemorrhagic shock stems
from a systemic inflammatory response. Unlike sepsis, the systemic
inflammation after hemorrhagic shock is not due to a specific
site of infection. Instead, other stimuli activate inflammatory
pathways. Examples include hypoxia, release of circulating factors
such as hormones or changes in flow which are sensed locally and
initiate signaling cascades. We have previously shown that several
genes, include the inducible nitric oxide synthase (iNOS), CD14,
and COX-2 are all upregulated during shock alone. These findings
initiated a search for the upstream signaling pathways involved
in the activation of gene expression during shock.
