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Abstract

25 ALI = acute lung injury; ARDS = acute respiratory distress syndrome; BAL = bronchoalveolar lavage; fMLP = formyl-methionyl-leucyl-phenylalanine; IL = interleukin; KGF = keratinocyte growth factor; LPS = lipopolysaccharide; SP = surfactant protein; TNF = tumour necrosis factor. [1]. Morbidity among survivors is also high, with persistent functional limitation 1 year after discharge preventing over half from returning to work [6].Improvements in general supportive care have contributed toward a trend of decreasing mortality over the past 10 years [7], and recently strategies to reduce the effects of ventilatorassociated lung injury have resulted in an important reduction in mortality [8]. However, as yet no specific pharmacological therapies to target the underlying pathological processes have proved efficacious [9]. Recent in vitro and in vivo animal or human studies suggest that β 2 -agonists -drugs that are well established in the management of patients with chronic bronchitis or asthma -may have an important therapeutic role to play in modulating the initial inflammatory insult and enhancing alveolar fluid clearance in patients with ARDS.The present review discusses the effects of β 2 -agonists on neutrophil functions, on inflammatory mediators, and on epithelial and endothelial functions (Fig. 1). It draws on the extensive experimental and clinical literature on the mechanisms of effects of β 2 -agonists to suggest a potential role for their use as a specific pharmacological intervention in patients with ARDS. ReviewBench-to-bedside review: β β 2 -Agonists and the acute respiratory distress syndrome AbstractThe acute respiratory distress syndrome (ARDS) is a devastating constellation of clinical, radiological and pathological signs characterized by failure of gas exchange and refractory hypoxia. Despite nearly 30 years of research, no specific pharmacological therapy has yet proven to be efficacious in manipulating the pathophysiological processes that underlie this condition. Several in vitro and in vivo animal or human studies suggest a potential role for β 2 -agonists in the treatment of ARDS. These agents have been shown to reduce pulmonary neutrophil sequestration and activation, accelerate alveolar fluid clearance, enhance surfactant secretion, and modulate the inflammatory and coagulation cascades. They are also used widely in clinical practice and are well tolerated in critically ill patients. The present review examines the evidence supporting a role for β 2 -agonists as a specific pharmacological intervention in patients with ARDS.

The Effect of Inhaled Salbutamol in Transient of Tachypnea of the Newborn: A Randomized Clinical Trial

“…Recent studies conducted to investigate the efficacy of intravenous administration of albuterol (salbutamol), a beta 2 A, on pulmonary edema models both in-vitro and in-vivo in adult patients, supported the evidences that beta 2 A could be an efficient pharmacological intervention in patients with acute respiratory distress syndrome (21,22). On the other hand, the positive protective effect of beta 2 A receptor signaling on alveolar active Na transport in normal and injured lung provides substantial support for the use of beta 2 A agonist to accelerate alveolar clearance in TTN (16).…”

Increased cardiac index due to terbutaline treatment aggravates capillary-alveolar macromolecular leakage in oleic acid lung injury in dogs

“…Indeed β-agonists are known for their anti-inflammatory effects and for improving the tightness of the endothelial cells [7,8]. …”

The rise and fall of β-agonists in the treatment of ARDS

“…A number of mechanisms have been proposed by which ion transport is increased by raised cAMP levels, including a greater sodium channel open probability, changes in the phosphorylation of the Na + -K + -ATPase α-subunit, greater delivery of ENaC and Na + -K + -ATPase, and increased chloride transport by the cystic fibrosis transmembrane conductance regulator [6,10]. …”

“…β-adrenoceptor agonists (β-agonists) are well established in the treatment of airflow obstruction. In addition to actions as bronchodilators, they have anti-inflammatory properties, promote the clearance of alveolar fluid, and promote epithelial and endothelial repair [6]. The scientific rationale for a potential role in the treatment of ARDS is summarized in Figure 1.…”