ABSTRACT
Sepsis is a systemic inflammatory response syndrome in the presence of suspected or proven infection; and it may progress to or encompass organ failure (severe sepsis) and hypotension (septic shock). Clinicians possess an arsenal of supportive measures to combat severe sepsis and septic shock; and some success; albeit controversial; has been achieved by using low doses of corticosteroids or recombinant human activated protein C. However; a truly effective mediator-directed specific treatment has not been developed yet. Treatment with low doses of corticosteroids or with recombinant human activated protein C remains controversial and its success very limited. Attempts to treat shock by blocking LPS; TNF or IL-1 were unsuccessful; as were attempts to use interferon-gamma or granulocyte colony stimulating factor. Inhibiting nitric oxide synthases held promise but met with considerable difficulties. Scavenging excess nitric oxide or targeting molecules downstream of inducible nitric oxide synthase; such as soluble guanylate cyclase or potassium channels; might offer other alternatives
Subject(s)
Adrenal Cortex Hormones , Nitric Oxide , Protein C , Sepsis/therapyABSTRACT
Sepsis is a systemic inflammatory response syndrome in the presence of suspected or proven infection; and it may progress to or encompass organ failure (severe sepsis) and hypotension (septic shock). Clinicians possess an arsenal of supportive measures to combat severe sepsis and septic shock; and some success; albeit controversial; has been achieved by using low doses of corticosteroids or recombinant human activated protein C. However; a truly effective mediator-directed specific treatment has not been developed yet. Treatment with low doses of corticosteroids or with recombinant human activated protein C remains controversial and its success very limited. Attempts to treat shock by blocking LPS; TNF or IL-1 were unsuccessful; as were attempts to use interferon-gamma or granulocyte colony stimulating factor. Inhibiting nitric oxide synthases held promise but met with considerable difficulties. Scavenging excess nitric oxide or targeting molecules downstream of inducible nitric oxide synthase; such as soluble guanylate cyclase or potassium channels; might offer other alternatives