|
HYPERBARIC OXYGEN THERAPY IN THE TREATMENT
OF BURNS:
EVALUATION OF SYSTEMIC LIPID PEROXIDATION AND
ACTIVATION OF OXYGEN-RADICAL DEPENDENT INFLAMMATORY REACTIONS
P.Germonpré (1), I. Van Renterghem (1),
P.Reper (2), L.Duinslaeger (2), A.Vanderkelen (2)
(1) Center for Hyperbaric Oxygen Therapy, Military Hospital Brussels
(2) Burn Center, Military Hospital Brussels
Introduction
In a previous study, we demonstrated the ability of Hyperbaric
Oxygen Therapy (HBOT) to prevent at least partially the deepening
of an experimental burn during the first days after injury. However,
most of the distant complications of major burns seem to be related
to the generation of Oxygen Free Radicals (OFR). Therefore, before
proceeding to a clinical human study, we wanted to evaluate the
possible toxic effects of HBOT in a more extensive burn injury.
Methods
A double-blind prospective study was undertaken. Male Wistar
rats were subjected to a 40% TBSA thermal burn or sham burn by
submersion, and were resuscitated with intraperitoneal Hartmann
solution. After randomisation, half of the burned animals received
one HBOT session (60 minutes, 2 ATA) starting 30 minutes after
the burn. The animals were sacrificed at 30 minutes (sham burn
and control burn groups), 120, 240 or 360 minutes (all groups).
Lipid peroxidation products were measured by means of an optimised
fluorometric measurement of Malondialdehyde (MDA). Systemic inflammation
was evaluated using standard Complement Hemolytic Activity (CH50)
and Tumor Necrosis Factor alpha (TNFa).
Results
There was a significant difference in the mortality rate at time
points 240 and 360: 28% in the control burn group vs. 11% and
7% in the sham burn groups and HBOT groups respectively. The serum
MDA content in the HBOT treated rats was similar to that of the
sham burned rats, at all time points, whereas the control burn
rats showed a moderate but significant rise at time points 120
and 240 (p<0.05). The HBOT group showed normal CH50 values
at all time points, whereas the control burn group showed a stimulation
of complement activation and production (but not depletion), reflected
by a rise in CH50 (p<0.05). There was a small and statistically
non-significant rise in serum TNFa content (p>0.05).
Conclusions
Early HBOT seems to diminish the generation of lipid peroxidation
products after a 40% TBSA experimental burn. It seems moreover
to have a positive effect on complement activation, and no significant
influence on TNFa production. We conclude that, in this model,
HBOT seems a safe therapeutic procedure.
(Supported by a grant from the Brussels Capital
Region Energy Department)
|