Review
Copyright ©2012 Baishideng. All rights reserved.
World J Crit Care Med. Apr 4, 2012; 1(2): 50-60
Published online Apr 4, 2012. doi: 10.5492/wjccm.v1.i2.50
Acute respiratory distress syndrome and lung injury: Pathogenetic mechanism and therapeutic implication
Chain-Fa Su, Shang Jyh Kao, Hsing I Chen
Chain-Fa Su, Department of Neurosurgery, Tzu Chi University Hospital, Hualien 97004, Taiwan, China
Shang Jyh Kao, Division of Chest Medicine, Department of Internal Medicine, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei 110, Taiwan, China
Shang Jyh Kao, School of Respiratory Therapy, Taipei Medical University, Taipei 110, Taiwan, China
Hsing I Chen, Institute of Physiological and Anatomical Medicine, Tzu Chi University, Hualien 97004, Taiwan, China
Author contributions: Su CF was responsible for the portions of neurogenic pulmonary edema; Kao SJ contributed to the clinical investigations of acute respiratory distress syndrome; Chen HI organized the whole review article and finalized the manuscript writing.
Supported by Grants from the National Science Council, Far-Eastern Medical Foundation; and Tzu Chi Charitable Foundation
Correspondence to: Hsing I Chen, MD, PhD, Professor, Institute of Physiology and Anatomical Medicine, Tzu Chi University, Hualien 97004, Taiwan, China. chenhi@mail.tcu.edu.tw
Telephone: +886-3-8560824 Fax: +886-3-8573075
Received: September 27, 2011
Revised: October 14, 2011
Accepted: March 10, 2012
Published online: April 4, 2012
Abstract

To review possible mechanisms and therapeutics for acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). ALI/ARDS causes high mortality. The risk factors include head injury, intracranial disorders, sepsis, infections and others. Investigations have indicated the detrimental role of nitric oxide (NO) through the inducible NO synthase (iNOS). The possible therapeutic regimen includes extracorporeal membrane oxygenation, prone position, fluid and hemodynamic management and permissive hypercapnic acidosis etc. Other pharmacological treatments are anti-inflammatory and/or antimicrobial agents, inhalation of NO, glucocorticoids, surfactant therapy and agents facilitating lung water resolution and ion transports. β-adrenergic agonists are able to accelerate lung fluid and ion removal and to stimulate surfactant secretion. In conscious rats, regular exercise training alleviates the endotoxin-induced ALI. Propofol and N-acetylcysteine exert protective effect on the ALI induced by endotoxin. Insulin possesses anti-inflammatory effect. Pentobarbital is capable of reducing the endotoxin-induced ALI. In addition, nicotinamide or niacinamide abrogates the ALI caused by ischemia/reperfusion or endotoxemia. This review includes historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS.

Keywords: Acute lung injury; Acute respiratory distress syndrome; Pathogenetic mechanisms; Therapeutic regimen; Nitric oxide; Inducible nitric oxide synthase