Data from: Neuroprotection provided by hypothermia initiated with high transnasal flow with ambient air in a model of pediatric cardiac arrest

Clinical trials of hypothermia after pediatric cardiac arrest have not
seen robust improvement in functional outcome, possibly because of the
long delay in achieving target temperature. Previous work in infant
piglets showed that high nasal airflow, which induces evaporative cooling
in the nasal mucosa, reduced regional brain temperature uniformly in half
the time needed to reduce body temperature. The mouth is kept open to
allow the high nasal airflow to easily exit. Here, we evaluated whether
initiation of hypothermia with high transnasal airflow (32 L/min) provides
neuroprotection without adverse effects in the setting of asphyxic cardiac
arrest. Anesthetized, mechanically ventilated piglets (approximately
2-weeks-old) underwent sham-operated procedures (Group 1) or asphyxic
cardiac arrest (Groups 2-6). The asphyxic insult consisted of reducing the
inspired oxygen from 30% to 9.5-10% for 45 minutes (hypoxia period), then
briefly increasing the inspired oxygen to 21% for 5 min (to improve the
later success of cardiac resuscitation), and then completely stopping
ventilation for 7 minutes. Cardiopulmonary resuscitation (CPR) commenced
by re-establishing ventilation, performing chest compression, and
injecting epinephrine as needed. The five cardiac arrest groups were
further divided into those with normothermic recovery (38.5°C; Group 2),
with mild hypothermia (34°C) initiated by surface cooling at 10 minutes
(Group 3) or 120 minutes (Group 5) after resuscitation, or with mild
hypothermia (34°C) initiated by transnasal cooling initiated at 10 minutes
(Group 4) or 120 minutes (Group 6) after resuscitation. In the two
transnasal cooling groups, the high nasal airflow continued for 2 hours
and was then stopped; thereafter, surface cooling was used to maintain
hypothermia. In all four groups with induced hypothermia, rectal
temperature was sustained at the targeted temperature of 34°C with surface
cooling until 20 hours after resuscitation, followed by 6 hours of gradual
rewarming and cessation of fentanyl/70% nitrous oxide anesthesia. At four
days of recovery, the piglets were euthanized and their brains were
analyzed for the density of morphologically intact neurons in putamen,
sensorimotor cortex, ventrolateral thalamus, and prefrontal cortex. The
data sheet shows the density of viable neurons in these 4 brain regions
for the 45 piglets that completed the study. The data sheet also shows the
serial measurements of rectal temperature, mean arterial blood pressure,
heart rate, and arterial blood measurements of the partial pressure of
oxygen (PO2) and carbon dioxide (PCO2), oxyhemoglobin saturation, and pH
obtained at baseline, during the period of hypoxia, at 4 minutes of
ventilation with 21% O2, during the period of asphyxia, and during the
first 24 hours of recovery. The piglets are assigned the same unique
identifier number, labelled 1-45, for each set of measurements. Transnasal
cooling initiated at 10 minutes after resuscitation was able to
significantly rescue neurons in the highly vulnerable putamen without
adverse effects.