After reviewing the characteristics of neurogenic pulmonary edema, Theodore and Robin suggested that it was probably due to rupture of lung vessels by marked but transitory pulmonary hypertension. In this study, we have determined the effects of increased intracranial pressure in a sheep model in which we could measure the flow rate and protein content of lung lymph, and thus detect changes in pulmonary vascular permeability. We found that increasing intracranial pressure to amounts near systemic arterial pressure produced a 3-fold increase in the flow of protein-rich lymph, which indicates increased lung vascular permeability. The high permeability often developed, and always persisted, without extraordinary increases in pulmonary vascular pressure. We conclude that increased lung vascular permeability may follow intracranial hypertension and that extreme pulmonary hypertension is not a prerequisite. Our data do not permit us to exclude barotrauma to exchanging vessels as a cause of capillary damage, but do suggest that other factors, perhaps local release of permeability mediators, may be involved.