Low hematocrit worsens cerebral injury after prolonged hypothermic circulatory arrest in rats.

Purpose: This study tests the hypothesis that low hematocrit (Hct) worsens cerebral injury after prolonged hypothermic circulatory arrest (HCA) in rats, and the mechanism involves variable expression of the genes C-Fos, Bcl-2 and Bax.

Methods: A rat HCA model was developed, and 40 animals were randomly assigned to four groups: Sham (sham) group, or Hct groups of Hct 10%, Hct 20% and Hct 30%. After 90 min of HCA at 18 degrees C, physiologic variables were recorded and brain morphological changes were evaluated with light and electron microscopy. Expressions of C-Fos, Bcl-2, Bax in various brain areas were measured by the reverse transcriptase polymerase chain reaction and standard immunohistochemistry techniques.

Results: The number of injured neurons in the hippocampus CA1 and parietal cortex in the Hct 10% group (CA1: 11.44 +/- 2.52; cortex: 13.65 +/- 2.31) exceeded the mean number of injured neurons in the Hct 20% group (CA1: 8.29 +/- 1.31; cortex: 10.68 +/- 1.24; P < 0.05) and the Hct 30% group. Mean mitochondrial injury scores were greatest at lower Hct levels, while the expression of C-Fos and Bax were highest in the Hct 10% group and lowest in the Hct30% group (P < 0.05). In contrast, the expression of the Bcl-2 mRNA was greatest in the Hct 30% group (P < 0.05).

Conclusion: Low Hct worsens cerebral injury after prolonged HCA and CPB in rats, which may relate in part to the variable expression of the genes C-Fos, Bcl-2 and Bax.