Prolonged cooling duration mitigates myocardial and cerebral damage in cardiac arrest

The purpose of this study was to investigate the effect of prolonged cooling on cardiac and cerebral injury in animals under cardiac arrest.

Adult male Wistar rats were equally randomized to normothermia, 5H1, 5H2, 7H1, 7H2, and 7H4 groups. The first number in the group name indicated ventricular fibrillation duration (minutes), the middle H indicated hypothermia, and the last number signified hypothermia duration (hours). Ventricular fibrillation was induced and untreated for 5 minutes (normothermia, 5H1, and 5H2) or 7 minutes (7H1, 7H2, and 7H4) followed by 1 minute of cardiopulmonary resuscitation followed by electric shocks. Hypothermia was initiated simultaneously with cardiopulmonary resuscitation initiation and maintained for 1 hour (5H1 and 7H1), 2 hours (5H2 and 7H2) or 4 hours (7H4).

There were 12 rats in each group. Compared with the 7H1 group, the 7H4 group had significantly better systolic function (dp/dt40) and cardiac output within the early postcardiac arrest period. Histologic examination disclosed less myocardial and hippocampal damage in the 7H4 group than the 7H1 group and in the 5H2 group than the 5H1 group. Plasma troponin I, fatty acid-binding protein, and S-100β concentrations were significantly lower in the 7H4 and 5H2 groups. The 7H4 and 5H2 groups survived statistically longer than the groups with shorter cooling duration.

Slightly prolonging hypothermia may mitigate myocardial and cerebral damage and improve survival and neurologic outcomes in a rat model of ventricular fibrillation cardiac arrest.