One of the earliest pathophysiological events in the pathogenesis of acute inflammatory lung injury is damage to the delicate pulmonary endothelium with a resultant breakdown in the alveolar-capillary barrier leading to flooding of the pulmonary interstitum and alveolar airspace with a protein rich fluid. Techniques have been developed which utilise externally situated gamma detectors to chart the transit of radiolabelled proteins from the intravascular space to the pulmonary interstitium which provide a non-invasive and dynamic measurement which is both sensitive to and specific for the detection of inflammatory pulmonary oedema. The aim of this thesis is to assess the applicability of a fully portable dual isotope system which utilises three miniature scintillation detectors in the recording of pulmonary microvascular permeability. Recordings will be carried out in the Intensive Care and High Dependency setting from patients both with established ARDS and from a group of patients at-risk of ALI/ARDS. In patients at-risk of ARDS I will examine the hypothesis that it is possible to identify a subgroup of patients in whom a subclinical inflammatory response will be associated with the emergence of pulmonary microvascular permeability. I will also investigate whether the occurrence of pulmonary permeability represents a forme fruste which fails to progress or whether it is a reliable indicator of impending severe lung injury. Furthermore, in both groups of patients I wish to investigate whether the occurrence of enhanced microvascular permeability may be correlated with key inflammatory markers which may support contentions for their role in the pathogenesis of lung injury and also provides a true or surrogate marker for the presence or absence of enhanced microvascular permeability.