Abstract
Acute lung injury is associated with a number of clinical conditions including endotoxic and septic shock, acute respiratory distress syndrome (ARDS) and pulmonary embolism. Despite improved therapy with steroids, aprotinin and dobutamine, mortality figures still remain high, being between 50 and 75% in patients with ARDS (1). The pathophysiology of shock and acute lung injury is very complex and still remains to be elucidated. The clinical symptoms characterising shock and acute lung injury are profound haemodynamic disturbances, in particular systemic hypotension associated with a fall in peripheral vascular resistance, pulmonary hypertension, bronchoconstriction and pulmonary oedema. Additionally, there are major alterations in circulating blood elements such as thrombocytopenia, leukopenia and systemic vascular permeability. Several animal models have been utilised in attempts to further understand the pathogenesis of lung injury. These models include exposure of animals to thrombin or fibrin derived peptides (2), hypoxia (3), and more commonly, endotoxin shock (4). In particular, infusion of Escherichia Coli into unanaesthetised sheep is a widely used model of endotoxic shock which reproduces several features of the human clinical syndrome. There is an early transient phase of pulmonary hypertension and increased resistence to air flow, followed by a prolonged phase with high flow of protein-rich lung lymph indicating increased permeability and pulmonary oedema (5).
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Page, C.P., Robertson, D.N. (1987). A Role For Platelet Activating Factor In Shock And Acute Lung Injury. In: Paubert-Braquet, M., Braquet, P., Demling, B., Fletcher, J.R., Foegh, M. (eds) Lipid Mediators in the Immunology of Shock. NATO ASI Series, vol 139. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0919-2_21
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DOI: https://doi.org/10.1007/978-1-4613-0919-2_21
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