Abstract

Artificial mechanical ventilation is a double-edged sword. Although indispensable in order to maintain oxygenation in patients it can also cause iatrogenic lung damage and may even have detrimental consequences in organs other than the lung. For a long time, research on the side-effects of mechanical ventilation had focused on physical forces and their effect on lung integrity [1]. Recently, we [2, 3] and others [4] have started to investigate the molecular mechanisms of ventilation-induced lung damage. These new findings suggest that ventilation at high volumes can act as a pro-inflammatory stimulus resulting in pulmonary production of tumor necrosis factor (TNF), interleukin-6 (IL-6) and other mediators. Such pro-inflammatory mediators represent potential candidates of initiating or promoting lung injury. Moreover, their release into the circulation may lead to development of the systemic inflammatory response syndrome (SIRS). It should be noted that this could elicit inflammatory responses in the absence of any infection.