Infusion of 4°C normal saline can improve the neurological outcome in a porcine model of cardiac arrest

Abstract

This study sought to investigate induction of therapeutic hypothermia using ice-cold intravenous fluid after cardiopulmonary resuscitation (CPR). The effects on temperature, hemodynamics, cognitive performance and the accompanying neurohistopathological changes, and apoptosis were assessed. Fourteen piglets had 4 minutes of untreated ventricular fibrillation, followed by CPR. The animals in which spontaneous circulation was restored were randomly assigned to two groups: the hypothermia group (n = 7) was given an infusion of 4°C cold normal saline solution 30 mL/kg at an infusion rate of 1.33 mL/kg/min, followed by 10 mL/kg/h to 4 hours after restoration of spontaneous circulation; the control group (n = 7) was given the same infusion at room temperature. Variables were measured repeatedly until 4 hours after restoration of spontaneous circulation. Neurocognitive performance was evaluated 24 hours after CPR. Then animals were killed and the brains were removed for histopathology at 24 hours after restoration of spontaneous circulation. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling method was used for apoptosis evaluation. Compared with the control group, the core temperature of the hypothermia group was significantly decreased (p < 0.01). The cerebral performance categories at 24 hours after restoration of spontaneous circulation in the hypothermia group were better than that in the control group (p < 0.05). The percentage of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling-positive cells in the cortex and dentate gyrus of the hippocampus were significantly reduced in the hypothermia group compared with the control group at 24 hours after restoration of spontaneous circulation. By observation of transmission electron microscopy, the neuron damages were significantly reduced in hypothermia group. 4°C normal saline solution is a safe and effective method to reduce brain damages and prevent apoptotic cell death after cardiac arrest.