Physiologic stress and cellular ischemia

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Abstract
Multiple organ system failure secondary to infection is the most frequent cause of late mortality after hemorrhage, burns, and trauma. Although multiple immunologic abnormalities have been identified following injury, blood loss, and tissue ischemia, the mechanisms that produce these alterations in T- and B-cell function have not been completely defined. Physiologic stress and ischemia result in increased release of neuroendocrine peptides and hormones, capable of affecting normal neuroendocrine-immunologic balance and producing immunosuppression. Tissue ischemia leads to increased expression of heat shock proteins by hypoperfused cells, which can alter T-cell function. Injury also is followed by the appearance of serum immunosuppressive factors, which have been shown to inhibit T- and B-cell function. Future therapies directed at these and other cellular and molecular abnormalities initiated by tissue hypoperfusion may reverse the immunosuppressed state in critically ill patients and lead to improved outcome in this setting.

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