A
cute
respiratory distress syndrome (ARDS) is a
major cause of
mortality
in critical
care
, but
to d
ate
no specific treatment exists.
There is growing concern about our
failure to translate from bench to bedside within the acute lung injury research
community,
and t
he crucial importance of better modelling
in
preclinical
studies
to
identify targets
with
more predictive
power
is increasingly
appreciated
.
Mechanical
ventilation
, while being a vital tool for
support of
ARDS
patients
,
produces or
worsens lung injury
. This ‘
ventilator
-­
induced lung injury
’
(
VILI
)
has
substantive
negative impact on
the
outcom
e
of ARDS
.
I
ncreasing tidal volumes are associated
with enhanced
release
of local and systemic inflammatory mediators
in
patients
,
and
a
nimal model
s d
emonstrated
that
excessive tidal volumes induce
lung
inflammation,
edema and physiological dysfunction.
Such findings have lent support to the
‘biotrauma’ hypothesis,
i.e.
VILI
promotes the release of
inflammatory
mediators
,
which
play a
critical
role in the progression of
injury of the lungs as well as
other
systemic
organs [1].
In
this issue
of Anesthesiol
ogy, Lex and Uhlig
[
2
]
investigate
whether this biotrauma
can be studied in
so
-­
called
‘one
-­
hit’ models of
VILI
in mice
.
Their
results
provide useful information
for physiologists
to
better
design
mouse
VILI
experiments, but more importantly,
p
rovoke a seri
es of
important
questions
that are
essential
for clinicians
desiring
to interpret animal
VILI
models
for
future
clinical
translation.