| Autor: |
Skikic, Maja, Guo, Shang Z., Reeves, Stephen R., Miller, James J., Gozal, David, Yang Wang |
| Předmět: |
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| Zdroj: |
FASEB Journal; Apr2007, Vol. 21 Issue 6, pA1278-A1278, 1/4p |
| Abstrakt: |
WHPC extends the survival of mice exposed to lethal environmental hypoxia by preserving structural and functional integrity of key organs. We now examined whether WHPC would also prolong survival in response to hemorrhagic shock. Conscious male rats were subjected to bleeding of 60% of their estimated blood volume (∼37.2 ml/kg) over 30 min. We found that naïve rats died 76+9 min after the completion of bleeding (n=15) and this process was associated with progressively increasing metabolic acidosis and cell/organ injury. In contrast, more than 80% of rats treated with WHPC (6 cycles of 8% O2x10-min/21% O2x10-min) 2 h before bleeding survived >6 h without fluid resuscitation (n=14, p<0.001) and displayed significantly reduced acidosis and cell/organ injury. Although it decreased drastically following bleeding in all rats, Oz consumption in those treated with WHPC was significantly higher, suggesting better tissue perfusion in these animals. Furthermore, surviving animals appeared to be recovering from the initial impact of massive blood loss, with accelerated compensation and sustained maintenance of key variables above critical levels (mean arterial pressure >60 mmHg, blood base excess >-6 mmol/L, and plasma lactate <5 mmol/L). WHPC treatment 8 h before bleeding was associated with similar beneficial effects. We conclude that WHPC provides a robust protective mechanism against acute hemorrhagic shock. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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