Cardiac arrest (CA) is a leading cause of mortality worldwide. Most of post-
resuscitation related deaths are due to
post-cardiac arrest syndrome (PCAS). After
cardiopulmonary resuscitation (
CPR), return of spontaneous circulation (ROSC) leads to renal
ischemia-reperfusion injury, also known as PCAS. Many studies have focused on brain and
heart injuries after ROSC, but
renal failure has largely been ignored. Therefore, we investigated the protective effects of
therapeutic hypothermia (TH) on asphyxial CA-induced renal injury in rats. Thirty rats were randomly divided into five groups: 1) the control group (
sham); 2) the normothermic CA (nor.); 3) a normothermic CA group that received TH immediately within 2 h after
CPR (Hypo. 2 hrs); 4) a normothermic CA group that received TH within 4 h after
CPR (Hypo. 4 hrs); and 5) a normothermia CA group that received TH within 6 h after
CPR (Hypo. 6 h). One day after
CPR, all rats were sacrificed. Compared with the normothermic CA group, the TH groups demonstrated significantly increased survival rate (P < 0.05); decreased serum blood
urea nitrogen,
creatinine, and
lactate dehydrogenase levels; and lower histological damage degree and
malondialdehyde concentration in their renal tissue.
Terminal deoxynucleotidyl transferase dUTP nick end labeling
stain revealed that the number of apoptotic cells significantly decreased after 4 h and 6 h of TH compared to the results seen in the normothermic CA group. Moreover, TH downregulated the expression of
cyclooxygenase-2 in the renal cortex compared to the normothermic CA group one day after
CPR. These results suggest that TH exerts anti-apoptotic, anti-inflammatory, and anti-oxidative effects immediately after ROSC that protect against renal injury.