Skip to content

Advertisement

  • Poster presentation
  • Open Access

Low hematocrit causes worsened cerebral injury after prolonged hypothermic circulatory arrest in rats: possible involvement of C-Fos, Bcl-2 and Bax

  • 1
Critical Care200610 (Suppl 1) :P229

https://doi.org/10.1186/cc4576

  • Published:

Keywords

  • Hematocrit Level
  • Cerebral Injury
  • Sample Brain Tissue
  • Gaining Insight
  • Sham Operation Group

Background

Although experience with cardiovascular surgery in adults refusing transfusion suggests that very low hematocrit levels can be tolerated, the optimal hematocrit level for cerebral protection during CPB and HCA has not been defined. Gaining insights into the cerebral consequences of HCA and CPB, and in particular the molecular pathways possibly involved, has been limited by the relative inability to study brain tissue after recovery from HCA and CPB. With the development of a rat model of CPB, we have been able to sample brain tissue after HCA and CPB for molecular analysis with well-established molecular tools. In this study, we hypothesized that low hematocrit causes worsened cerebral injury after prolonged hypothermic circulatory arrest in rats, with possible involvement of C-Fos, Bcl-2 and Bax.

Methods

A rat HCA model was developed and animals were randomly distributed into four groups: sham operation group (sham op); hematocrit (Hct) 10% group; Hct 20% group and Hct 30% group (n = 10 each). All animals except those of the sham op group underwent HCA for 90 min at 18°C. Physiologic values such as Hct, pH and so on were monitored. Brain damage after HCA was evaluated with the light microscopy and electron microscopy. RT-PCR and imunohistochemistry techniques were used to measure the transcription and translation of the C-Fos, Bcl-2 and Bax in various brain parts.

Results

After beginning CPB, Hct was decreased to the target levels. 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) was higher than that of the Hct 20% group (CA1: 8.29 ± 1.31; cortex: 10.68 ± 1.24; P < 0.05), and the Hct 20% group was higher than that of the Hct 30% group (CA1: 4.40 ± 1.98; cortex: 7.38 ± 2.11). The mean score of mitochondrial injury in the Hct 10% group (34.05 ± 1.56) was higher than that of the Hct 20% group (29.30 ± 0.68; P < 0.05) and the Hct 20% group was higher than that of the Hct 30% group (18.65 ± 0.53; P < 0.05). The ratio of mRNA transcription of C-Fos and Bax to that of β-actin in the Hct 10% group (C-Fos: 1.94 ± 0.19; Bax: 1.41 ± 0.12) was higher than that of the Hct 20% group (C-Fos: 1.66 ± 0.13; Bax: 1.22 ± 0.14, P < 0.05) and the Hct 20% group was higher than that of the Hct 30% group (C-Fos: 1.33 ± 0.16; Bax: 0.99 ± 0.14, P < 0.05). On the other hand, the transcription of the Bcl-2 mRNA in the Hct 30% group (0.97 ± 0.04) was higher than that of the Hct 20% group (0.76 ± 0.10) and the Hct 10% group (0.75 ± 0.12, P < 0.05). The numbers of C-Fos and Bax immunoreactive cells in the hippocampus CA1 and parietal cortex in the Hct 10% group (C-Fos in CA1: 14.00 ± 2.45; C-Fos in cortex: 18.67 ± 2.16; Bax in CA1: 22.50 ± 1.87; Bax in cortex: 24.33 ± 3.88) were higher than those of the Hct 20% group (C-Fos in CA1: 10.83 ± 1.94; C-Fos in cortex: 12.50 ± 1.87; Bax in CA1: 14.67 ± 2.94; Bax in cortex: 14.00 ± 2.83; P < 0.05), and the Hct 20% group was higher than that of the Hct 30% group (C-Fos in CA1: 5.83 ± 0.75; C-Fos in cortex: 7.50 ± 1.05; Bax in CA1: 10.83 ± 1.47; Bax in cortex: 9.17 ± 1.72; P < 0.05). The number of Bcl-2 immunoreactive cells in the HCT 30% group (CA1: 13.33 ± 2.16; cortex: 15.50 ± 1.87) was higher than that of the Hct 20% group (CA1: 11.00 ± 1.41; cortex: 11.83 ± 2.04) and the Hct 10% group (CA1: 9.33 ± 1.21; cortex: 9.67 ± 1.03, P < 0.05).

Conclusion

Low hematocrit resulted in evidence of worsened cerebral injury after prolonged HCA and CPB in rats, which is possibly due to the regulation of the C-Fos, Bcl-2 and Bax transcription and translations.

Authors’ Affiliations

(1)
Renji Hospital, Shanghai Jiaotong University, Shanghai, China

Copyright

© BioMed Central Ltd 2006

Advertisement