Effect of Nitric Oxide on Renal Function in Septic Shock

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Abstract
Nitric oxide is a central mediator in septic shock because of its ability to relax smooth-muscle cells in arterial walls1. High levels of nitrate, one of the metabolites of nitric oxide, can be found in the serum of hypotensive patients with sepsis2,3. Several important features of nitric oxide in septic shock are illustrated by the case of a liver-transplant recipient who had two episodes of septic shock due to gram-negative bacteria, during which we measured blood concentrations of endotoxin, cytokines, and metabolites of nitric oxide ( Table 1 ). A bout of septicemia due to Escherichia coli on June 27 was followed by a short period of hypotension, which was successfully treated with fluids. During this episode, an increase in cytokine levels above basal values was detected, and the concentrations of metabolites of nitric oxide were increased on the following days. On July 9, septic shock again developed and required treatment with vasoactive drugs in addition to volume loading. This treatment maintained the systolic blood pressure above 110 mm Hg. The cytokine profile during this period was similar to that reported during the first episode, whereas the concentrations of metabolites of nitric oxide were decreased. Oliguric renal failure ensued, and hemodialysis was required from July 11 until the patient's death on July 27.

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