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Journal of Applied Physiology, Vol 74, Issue 6 2782-2787, Copyright © 1993 by American Physiological Society
ARTICLES |
P. Carvalho, W. Kirk, J. Butler and N. B. Charan
Pulmonary Research Laboratory, Department of Veterans Affairs Medical Center, Boise, Idaho 83702.
We studied the pleural inflammatory response to tube thoracostomy by inserting an Argyle 32-Fr tube in the pleural space of 10 anesthetized sheep. An experimental pleural effusion was created by infusion of sterile normal saline (10 ml/kg) into the pleural space, and the animals were allowed to recover. Systemic blood and experimental pleural effusion (EPE) samples were obtained at time 0, 30 min, hourly for 6 h, and at 6-h intervals for a total of 48 h. EPE white cell count rose from 125 +/- 125 to 6,323 +/- 2,268/microliters (SE) at 6 h (P < 0.05) but showed marked variability at 42 and 48 h (P < 0.05), with values ranging from 8,000 to 22,000/microliters. The systemic white cell count rose from 5,195 +/- 914 to 9,640 +/- 1,110/microliters (P < 0.01) within the first 12 h and then remained stable. EPE protein increased from 0 +/- 0 to 3.73 +/- 0.2 g/dl at 48 h (P < 0.05). EPE lactate dehydrogenase rose from 44 +/- 12 IU/l to a peak of 638 +/- 55 IU/l at 24 h (P < 0.05). EPE glucose was significantly lower than serum glucose at 36, 42, and 48 h (P < 0.05). These data indicate that chest tube placement rapidly induces significant pleural inflammation and results in formation of a sterile exudate.
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