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,
MN.
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.
