Neuroprotective effect of deep hypothermic circulatory arrest with low priming volume: study in a rabbit model

The aim of the study was to investigate the possible neuroprotective effects of a low priming volume following deep hypothermic circulatory arrest (DHCA) in a rabbit model.

Rabbits were randomized into three groups: DHCA with low priming volume (Group L), DHCA with high priming volume (Group H), and sham-operated group (Group S). The priming volume of Groups L and H were 75 ml and 210 ml, respectively. The rabbits were simultaneously placed on CPB and brain microdialysis, cooled to 16 to 18 degrees C with DHCA for 60 minutes. Physiological parameters were regularly recorded. The extracellular levels of glutamate, glucose, lactate, and pyruvate in the hippocampus were collected by microdialysis and measured by HPLC and a microdialysis analyzer. Brain damage was evaluated with light microscopy and electron microscopy and TUNEL staining.

In order to keep the mean arterial pressure and acid-base balance within defined physiological ranges, more doses of dopamine and sodium bicarbonate were administered in Group H than in Group L (P < 0.05). The ratios of lactate/glucose and lactate/pyruvate in Group H increased significantly compared with those in Group L from the beginning of weaning from CPB (P < 0.05). The levels of extracellular glutamate in the two DHCA groups increased significantly (P < 0.05). After weaning from CPB, the glutamate values in Group H remained at higher levels compared with those in Group L (P < 0.05). The percentage of injured neurons, TUNEL positive staining, and the mitochondria score of the hippocampus CA1 in Group H were significantly higher than in Group L (P < 0.05).

A low priming volume during DHCA could have a neuroprotective effect compared with a high priming volume.