Abstract
Patients with severe sepsis are often treated with vasoactive agents in an attempt to restore cardiovascular function. Catecholamines, either administered as part of sepsis therapy or endogenously released as part of the early host response to injury, can influence the activation of inflammatory pathways during severe infection. This brief review discusses current knowledge of the interactions between exogenous and endogenous catecholamines on the one hand, and inflammatory responses activated during sepsis on the other hand.
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