Abstract

There has been considerable research into the role of reactive oxygen species (ROS) and more recently reactive nitrogen species in critical illness during the past decade. These highly reactive, short-lived compounds are generated continuously in normal cellular metabolism. Initially thought of as merely by-products to be detoxified as quickly as possible by the body’s numerous antioxidants, it is now recognized that they have important regulatory functions. Nevertheless, it is a widely accepted theory that during critical illness, particularly the acute respiratory distress syndrome (ARDS) and sepsis, and during conditions of ischemiareperfusion, the increased production of reactive species overwhelms the defense systems resulting in oxidant stress. This may contribute significantly to the morbidity and mortality of these conditions. Although a compelling theory, attempts to improve outcome in the critically sick with antioxidants have generally failed. In this article we shall briefly review the evidence for oxidant stress in sepsis and ARDS. We will then focus on one aspect of ROS in critical illness — their possible role in apoptosis, which is increasingly recognized as a key process in the critically ill patient.

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