The most common cause of death in patients with sepsis or other forms of critical illness is deterioration in the function of multiple organs, now termed multiple organ dysfunction syndrome (MODS). Commonly affected organs include the lungs, liver, and kidneys, and the clinical manifestations of arterial hypoxemia, decreased pulmona-ry compliance, cholestatic jaundice, oliguria, and azotemia are familiar to all intensivists. Manifestations of central nervous system dysfunction, ranging from subtle alterations in mental status to frank coma, are also common in patients with sepsis. Derangements in gastrointestinal function, including loss of normal peristalsis (ie, ileus) and enterocytic barrier function, are also common, albeit difficult to quantify, manifestations of MODS. Although a fatal outcome in patients with sepsis and septic shock is virtually always accompanied by MODS, the histopathology of fatal sepsis is remarkably bland. For example, histological sections of liver or kidney tissue from patients dying from sepsis or septic shock occasionally show evidence of focal necrosis or apoptosis (" programmed cell death"), but massive loss of parenchymal mass is rarely observed [1]. Thus the physiological basis for organ dysfunction in sepsis remains a puzzling problem.