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outcomes. In contrast, hypothermia has a well-established
neuroprotective effect and serves as a potential confounder if it is
not accounted for during experimental studies. Transient hypo-
thermia is also common after stroke, although more so in experi-
mental studies as a transient side effect of anesthetics used for the
surgical procedure. Currently, maintaining normothermia in exper-
imental stroke models and in human stroke care is the standard
( 15, 16 ). In human stroke care, normothermia is typically main-
tained with acetaminophen or ibuprofen by their downregulation
of the cyclo-oxygenase pathways ( 28 ) or with the application of
surface cooling or warming as needed.
In small animals, thermoregulation is more challenging due to
their large body surface area to mass ratio. As basal metabolic rates
are inversely proportional to body mass, small animals tend to
heavily depend upon their basal metabolic rate to maintain normo-
thermia. A typical laboratory mouse with a mass of 30 g has a basal
metabolic rate approximately 13 times greater than a 450 kg thor-
oughbred horse per gram of tissue ( 17 ). Thus, attention must be
paid to maintain body temperature in the laboratory setting, where
the often anesthetized animal is not able to meet the metabolic
demands needed to maintain normothermia.
Most experimental stroke models involve surgical procedures
with an anesthetized animal. The perioperative period involving
removing the animals from their cages, administering anesthesia
and the postoperative period often introduce opportunities of tem-
perature dysregulation. These alterations in temperature are often
unintentional and typically go unrecorded. Monitoring tempera-
ture before, during, as well as after the procedure ensures that
there are no unexpected extremes in temperatures which may con-
found the results of the experiment.
In experimental stroke studies, monitoring core body temper-
ature is often taken as a surrogate for the value of most interest—
brain temperature. Monitoring rectal temperature in this setting
assumes that there is a high degree of correlation between the brain
and body temperatures—whether measured by rectal or intra-
abdominal recording. Colbourne and colleagues ( 29, 30 ) have
described the discordance between brain and core body tempera-
tures, indicating that rectal temperature does not clearly and faith-
fully predict brain temperature. In a review of 15 studies comparing
core to brain temperatures, all 15 studies found that brain
temperature was higher than all measures of core temperature with
a mean difference of 0.39-2.5°C ( 31 ). Moreover, there is evidence
that the use of rectal temperature probes actually induces a rise in
body temperature most likely due to stress-induced mechanisms
( 32 ). Therefore, the decision to monitor temperature in experi-
mental stroke studies must determine whether core body
temperature monitoring will suffi ce or if monitoring brain tem-
perature is a necessary aspect to increase validity. Experiments in
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