Objectives: Increasing human and laboratory evidence suggests that post-res
uscitative brain hypothermia reduces the pathologic consequences of brain i
schemia. Using a swine model of prolonged cardiac arrest, this investigatio
n sought to determine whether unilateral hypothermic carotid bypass was cap
able of inducing selective brain hypothermia and reducing neurohistologic d
amage. Methods: Ventricular fibrillation was induced in common swine (n = 1
2). After 20 minutes of cardiopulmonary arrest (without ventilatory support
or cardiopulmonary resuscitation), systemic extracorporeal bypass was inst
ituted to restore coronary and cerebral perfusion, followed by restoration
of normal sinus rhythm. Animals randomized to the normal brain temperature
(NBT) cohort received mechanical ventilation and intravenous fluids for 24
hours. The selective brain hypothermia (SBH) cohort received 12 hours of fe
moral/carotid bypass at 32 degreesC. The bypass temperature was then increa
sed one degree per hour until reaching 37 degreesC and continued at this te
mperature until completion of the protocol (24 hours). Histopathologic dama
ge was evaluated in two areas of the hippocampus. Results: Normal sinus rhy
thm was restored in all animals after the systemic (femoral/femoral) bypass
was initiated. Nasal temperature (surrogate measure of brain temperature)
remained higher than 37.0 degreesC throughout the 24-hour recovery period i
n the NBT animals. In the SBH cohort, right nasal temperature dropped to th
e mild hypothermic range (< 34 degreesC) two hours after institution of fem
oral/carotid bypass. This was maintained throughout the 12-hour cooling per
iod without hemodynamic compromise. There was a significant improvement in
the neurohistology scores in the CAI region of the hippocampus of the SBH t
reated animals as compared with those of the NBT cohort. Conclusions: Post-
resuscitative selective brain hypothermia reduced regional ischemic brain d
amage in swine with prolonged ventricular fibrillation.