2004 OPEN FORUM Abstracts
PHYSIOLOGICAL AND INFLAMMATORY RESPONSES IN A PORCINE MODEL OF VENTILATOR INDUCED LUNG INJURY.
Dana Simonson BA, Alexander Adams RRT, MPH, John
Marini MD, David Dries MD. HealthPartners/Regions Hospital, St.Paul,
Background: Ventilator induced lung injury (VILI) is caused by alveolar pressures that directly rupture lung tissue and, eventually, effect an inflammatory response. Such a response is indicated by the presence of cytokines in the affected lung tissue or in "spillover" of cytokines into lavaged fluid or peripheral blood. A preceding injury (priming factor or first hit) can accelerate an inflammatory process caused by VILI (second hit). We previously reported the pathophysiological effects of 6 hours of high-pressure ventilation in a porcine model of VILI that was augmented in animals that had received a thoracotomy. This is a follow-up report of cytokine assays from that study.
Methods: An injurious pressure of Ptp = 35 cm H2O was applied to 17 pigs over a 6 hour period. In 8 of the animals, a thoracotomy was performed to implant pressure-sensing wafers. At 2-hour intervals, blood was sampled from the femoral artery for assay of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-8 as determined by enzyme- linked immunosorbant assay (ELISA).
Results: As previously reported, there was significantly greater deterioration in oxygenation and compliance in the thoracotomy primed animals. The results for TNF-α and IL-6 are displayed below; IL-8 was not expressed.
Conclusions: We speculate that the study preparation (line placement, tracheostomy formation) caused initiation of an inflammatory response, as indicated by elevated TNF-α and IL-6in each group. Although animals receiving a thoracotomy had a slightly greater inflammatory response as noted by differences in initial and developing IL-6 levels, we did not find a strong association between our measures of physiological and inflammatory responses to VILI.