In order to study the factors responsible for edema formation in endotoxin lung injury, we studied the effects of endotoxin infusion in an isolated autolagous blood perfused pig lung. All animals were anesthetized, exsanguinated, and their lungs ventilated with an air, 5% CO2 mixture once perfusion was established. Measured variables were pulmonary artery pressure (P(pa)), left atrial pressure (P(1a)), and lung weight change, which was measured as the inverse of the perfusate reservoir weight. Flows remained constant. Left atrial pressure was varied by adjusting the height of the reservoir. Measurements were made during a control period and again following endotoxin administration into the PA when P(pa) had returned to near control levels. All animals receiving endotoxin demonstrated a marked PA pressor response. A separate group of animals received no endotoxin, but served to demonstrate stability of the model over time. Cyclo-oxygenase mediators (T(x)B2 and 6-keto PGFl(α)) remained low in this group, but increased markedly in animals receiving endotoxin. Control and endotoxin group means were analyzed before and after endotoxin and at 0 and +5 P(1a) by analysis of variance. Endotoxin increased edema formation markedly when P(1a) was positive (p<.01), reflecting increased fluid filtration of the pulmonary vasculature when recruited. This model was developed to investigate pharmacologic interventions which might inhibit this response.
|Original language||English (US)|
|Pages (from-to)||No. 8727|
|State||Published - Jan 1 1985|
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