It is becoming increasingly apparent that lung and brain represent an integrated physiological ensemble such that insults involving one will compromise the other and vice versa [102] . Severe neurological injury is associated with concurrent lung injury in clinical settings. Recent studies have shown that acute lung injury may be responsible for brain injury and poor neurocognitive outcomes. However, the underlying biological mechanisms are yet to be elucidated. Heuer et al. [103] evaluated the independent and combined effects of sustained acute intracranial hypertension (AICH) and ARDS on lung injury and brain damage in a porcine model. They observed that markers of lung injury were augmented with AICH and rose further with concurrent AICH/ARDS. These observations shed valuable light on the complex process of signaling, involving neural, inflammatory, immunological, and neuroendocrine pathways. The fundamental physiological mechanisms still need to be addressed in future studies investigating whether the brain injury was due to increased capillary permeability, and whether the brain edema was vasogenic or cytotoxic. Given the significant epidemiologic and mechanistic overlap between sepsis and ALI/ARDS, it seems plausible that some of the known effects of sepsis on the brain may be relevant to brain dysfunction encountered in ALI/ARDS [102] .