Abstract

This study by Tanita and coworkers adds to a growing body of literature implicating activation of polymorphonuclear leukocytes (PMNs) as a contributing factor to pulmonary dysfunction. Using an isolated perfused rat lung model, the authors have investigated the impact of perfusion with human PMNs mechanically stimulated by gentle agitation in a glass vial. This resulted in increased CD18 integrin expression, assessed by immunofluorescence. The authors attempted to quantify capillary leak by modifying a method originally described by Aubrey Taylor’s group at the University of South Alabama. Capillary filtration coefficient has been used to quantify capillary leak in isolated perfused lung models for many years. It is based on the assumption that fluid leak into the lung interstitium is related to changes in intravascular pressure at the capillary level and the integrity of the endothelial membrane. In the classic model described by Taylor, isolated lung blocks are perfused while suspended from a force transducer until a steady state (constant weight) is achieved. Elevation of the venous reservoir results in increasing “back pressure” in the capillary circulation. Because the entire hydrostatic column may not be transmitted directly to the capillary bed (due to venous resistance), a double occlusion technique is generally used to quantify the increase in capillary pressure. In extensive studies in a variety of animals, Taylor’s group has demonstrated the reliability and reproducibility of the model.

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