Improving survival by increasing lung edema clearance: is airspace delivery of dopamine a solution?

Ariel Jaitovich,Jacob Sznajder

doi:10.1186/cc6825

Abstract

In this issue of Critical Care Chamorro-Marin and coworkers provide new evidence that dopamine instilled into airspaces is beneficial in a rat model of ventilator-induced lung injury. This study is important because it is the first to explore the effects of dopamine on survival, albeit short term. The delivery of dopamine into the airspaces in vivo is also novel and builds upon previous studies describing the mechanisms by which dopamine exerts its effect by upregulating active Na+ transport in the lungs. Dopamine appears to increase active Na+ transport via activation of amiloride-sensitive sodium channels and the basolateral Na+/K+-ATPase within minutes, and it has been shown to be effective in normal lungs and several models of lung injury. This information is relevant to current clinical trials exploring the effects of alveolar fluid clearance stimulation in patients with acute lung injury.

Highlights

In this issue of Critical Care Chamorro-Marin and coworkers [1] reported a significant decrease in short-term ventilatorinduced lung injury (VILI)-related mortality by intratracheal administration of dopamine in rats subjected to injurious mechanical ventilation
VILI occurs when the lung tissue is disrupted by high tidal volumes during mechanical ventilation, leading to pulmonary edema and hypoxemia [2]
In their study in rats, Chamorro-Marin and coworkers [1] found that administration of dopamine in airspaces exposed to injurious mechanical ventilation resulted in lower lung wet weight/dry weight ratio and improved survival in the dopamine-treated group

Summary

Introduction

In this issue of Critical Care Chamorro-Marin and coworkers [1] reported a significant decrease in short-term ventilatorinduced lung injury (VILI)-related mortality by intratracheal administration of dopamine in rats subjected to injurious (high tidal volume) mechanical ventilation. VILI occurs when the lung tissue is disrupted by high tidal volumes during mechanical ventilation, leading to pulmonary edema and hypoxemia [2].

Results

Conclusion