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Sepsis continues to be a major cause of patient death following hemorrhagic shock. To explain this increased susceptibility to infection on a cellular level, neutrophil function was studied in nine adult baboons subjected to severe hemorrhage. Neutrophil migratory activity was found to be significantly decreased immediately after hemorrhage (P less than 0.05 vs control) and continued to decline throughout the experiment. After an initial small decline, neutrophil adherence increased to significant levels after 4 h of hypotension (P less than 0.05 vs control). The present data support the hypothesis that increased susceptibility to infection after sustained hemorrhage is a result of impaired neutrophil function.
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