Future Clinical Trials of Pharmacologic Interventions

Abstract

Acute respiratory distress syndrome (ARDS) was first described as a clinical entity by Ashbaugh and Petty more than 25 years ago [1]. Since that initial description, there has been growing understanding of the pathophysiologic mechanisms which lead to the development of acute lung injury (ALI) in patient populations at risk. In particular, the roles of proinflammatory cytokines, chemokines, adhesion molecules, and oxygen radicals as mediators of pulmonary inflammation have been characterized. Alterations in neutrophil function, as well as the role of the neutrophil in damaging the lung and contributing to the development of ARDS and ALI have been described. Other chapters in this book have reviewed the mediators and cellular factors which contribute to the development of acute inflammatory lung injury, so that further discussion of the pathophysiology of ARDS is not required in this chapter. Rather, I will try to assess therapeutic approaches to ARDS and ALI which may be beneficial in the next 15 years.