Severe neurological dysfunction and injury are associated with a propensity to develop concurrent pulmonary edema and lung injury which can further worsen clinical outcomes [1]. This has been observed in a range of settings including traumatic brain injury [2], aneurysmal subarachnoid hemorrhage [3], status epilepticus [4], and in brain death [5]. More recently, studies have shown that critical pulmonary disorders such as acute lung injury and acute respiratory distress syndrome (ALI/ARDS) may be responsible for brain injury and poor neurocognitive outcomes [6, 7]. While the implications of these findings are considerable, the underlying biological mechanisms need clarification.In this issue of Intensive Care Medicine, Heuer et al.[8] use a porcine model to evaluate the independent and combined effects of sustained acute intracranial hypertension (AICH) and experimental ARDS on measures of lung injury and brain damage. They noted that markers of lung injury were augmented with AICH and further rose with concurrent AICH/ARDS. Moreover, measures of cerebral damage were increased in ARDS and even more elevated in combined AICH/ARDS. The study is remarkable if only because of its comprehensive design and the generous array of methods used to assess organ function and tissue injury including physiological measures (intracranial pressure, brain tissue pO 2 , heart rate variability, transpulmonary thermodilution), radiological assessments (quantitative brain and lung CT), biological markers (neuron-specific enolase, S100beta, cytokines), and histopathological analysis of lung and brain tissue. To our knowledge, it is one of the first studies to systematically address and quantify the independent and additive effects of neurological and lung injury. Limitations of this work must also be acknowledged. The balloon/AICH model is physiologically remote from traumatic brain injury in which the preponderance of damage is diffuse, not focal, and in which ICP elevations are generally paroxysmal in nature, not constant. Second, the animals were killed after only 4 h, resulting in a loss of valuable information on the natural history of AICH and/or ALI/ARDS in this model. Third, while increased edema was observed in both brain and lung, the available data do not address the underlying physiologic mechanism: was the pulmonary edema hydrostatic or due to increased capillary permeability? Was the brain edema vasogenic or cytotoxic in nature? It has been suggested that pulmonary edema following brain injury is in large part mediated via unbalanced catecholamine release resulting in pulmonary venous constriction and/or left ventricular failure [9, 10]; however, Heuer et al. do not clarify these aspects.It is becoming increasingly apparent that lung and brain represent an integrated physiological ensemble such that insults involving one will compromise the other and