Biphasic Onset of Splenic Apoptosis Following Hemorrhagic Shock
Author Information
Author(s): Arwed Hostmann, Kerstin Jasse, Gundula Schulze-Tanzil, Yohan Robinson, Andreas Oberholzer, Wolfgang Ertel, Sven K Tschoeke
Primary Institution: Charité – University Medical School Berlin
Hypothesis
The magnitude of cellular or parenchymal injury after trauma hemorrhage may be attributed, in part, to the rate of apoptosis induced by the respective event.
Conclusion
Hemorrhagic shock induces apoptotic changes in the spleen through a biphasic mechanism, leading to post-traumatic immunosuppression.
Supporting Evidence
- HS was associated with distinct lymphocytopenia as early as t = 0 hours after hemorrhage.
- A rapid activation of splenic apoptosis in HS mice was observed at t = 0 hours and t = 72 hours after hemorrhage.
- Expression of the anti-apoptotic Mcl-1 protein shows a significant increase at t = 24 hours compared with sham-operated and control animals.
- Bax and Bcl-2 proteins were inversely expressed within the 72-hour observation period.
Takeaway
When mice experience severe blood loss, their spleens start to die in two waves, which can make them more vulnerable to infections.
Methodology
Male C57BL-6 mice were subjected to sham operation or resuscitated hemorrhagic shock, and their spleens were evaluated for apoptotic changes at different time points.
Potential Biases
Potential bias in the selection of animal models and the interpretation of apoptotic markers.
Limitations
The study was conducted on a murine model, which may not fully replicate human responses to hemorrhagic shock.
Participant Demographics
Male C57BL-6 mice aged 8 to 12 weeks.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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