AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 5 1133-R1140, Copyright © 1991 by American Physiological Society
Plasma profiles of IL-6-like and TNF-like activities in brain-dead dogs
T. S. Huber, M. J. Kluger, S. P. Harris and L. G. D'Alecy
Department of Physiology, University of Michigan Medical School, Ann Arbor 48109-0622.
The progression to somatic death after brain death is poorly understood.
The role of tumor necrosis factor (TNF) and interleukin-6 (IL-6) in this
progression is unknown. TNF-like and IL-6-like plasma activities were
assayed in a canine model of brain death in the presence and absence of a
lipopolysaccharide (LPS) challenge (0.22 micrograms/kg). Bioassays for
TNF-like and IL-6-like activities used WEHI and B9 cell lines,
respectively. Brain death was induced by elevating and maintaining
intracranial pressure above systolic arterial pressure. Anesthesia and the
operative procedure did not cause a significant increase of either
cytokine. Brain death (n = 8) itself did not cause a significant elevation
of either cytokine compared with the sham brain-death control (n = 6)
despite a significant decrease in mean arterial pressure (35 +/- 3 vs. 115
+/- 5 mmHg at 5 h). The brain-dead group treated with LPS (n = 6) responded
with a significant elevation in IL-6-like and TNF-like activities compared
with the vehicle-treated group. The rise of IL-6-like activity in response
to LPS was greater in the brain-dead group than in the sham brain-dead
group (n = 3); no significant difference was noted for the TNF-like
response. We conclude that the progression to somatic death after brain
death cannot be explained by increases in circulating TNF-like or IL-6-like
activities.(ABSTRACT TRUNCATED AT 250 WORDS)
