Effects of therapeutic hypothermia on cerebral tissue oxygen saturation in a swine model of post-cardiac arrest

Since the introduction of therapeutic hypothermia (TH), trends have changed in the monitoring indicators used during and after cardiac arrest. During hypothermia, the cerebral metabolic rate of oxygen is reduced, which leads to uncertainty in regional cerebral tissue oxygen saturation (S(ct)O(2)). The aim of the present study was to evaluate the effect of TH on changes in S(ct)O(2) using near-infrared spectroscopy. A total of 23 male domestic pigs were randomized into three groups: TH (n=9), normothermia (NT; n=9) and control (n=5). Animals in the control group underwent surgical preparation only. The animal models were established using 8 min of ventricular fibrillation and 5 min of cardiopulmonary resuscitation. In the TH group, at 5 min after resuscitation, the animals were cooled with a cooling blanket and ice packs for 24 h. S(ct)O(2) was recorded throughout the experiment. In all groups, The mean arterial pressure, arterial carbon dioxide partial pressure, arterial oxygen partial pressure, lactate, neuron-specific enolase (NSE) and S100B were measured at baseline and at 1, 3, 6, 12, 24 and 30 h after resuscitation. S(ct)O(2) significantly decreased after ventricular fibrillation, compared with the baseline. Following resuscitation, the S(ct)O(2) values gradually increased to 55.6±3.8% of baseline in the TH group and 51.2±3.5% in the NT group (P=0.039). Significant differences between the two groups were observed, starting at 6 h after cardiac arrest. Throughout the hypothermic period, NSE and S100B showed an increasing trend, then decreased during rewarming in the TH and NT groups. NSE and S100B showed greater improvement in the TH group compared with the NT group at 6 and 24 h after resuscitation. Following cardiac arrest, therapeutic hypothermia could increase S(ct)O(2) after resuscitation and could improve neurological outcome. In conclusion, S(ct)O(2) may be a feasible marker for use in the early assessment of brain damage during and after cardiac arrest.