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Hemoglobin-based oxygen carrier attenuates cerebral damage by improving tissue oxygen preload in a dog model of
1Department of Anesthesiology and Translational Neuroscience Center, West China Hospital, Sichuan University , Chengdu, Sichuan , P. R. China.
Insights
Hemoglobin-based oxygen carriers (HBOCs) may reduce brain damage following cardiopulmonary bypass (CPB). This study found HBOCs improved oxygen levels and decreased brain injury biomarkers during CPB in dogs.
Area of Science:
- Cardiovascular Surgery
- Neuroprotection
- Biomedical Engineering
Background:
- Cardiopulmonary bypass (CPB) can induce cerebral damage.
- Effective neuroprotective strategies are crucial during CPB procedures.
Purpose of the Study:
- To investigate the neuroprotective effects of hemoglobin-based oxygen carriers (HBOCs) against CPB-induced cerebral injury.
- To determine if HBOCs can mitigate biochemical markers of brain damage post-CPB.
Main Methods:
- Male adult Beagle dogs were allocated to sham, control, or HBOC groups.
- A CPB model was established, involving 2 hours of cardiac arrest and 2 hours of reperfusion.
- Intracerebral oxygen tensions and biomarkers of cerebral damage were measured.
Main Results:
- HBOC administration improved intracerebral oxygen tensions.
- HBOCs significantly reduced the release of neuron-specific enolase and S100β in cerebrospinal fluid and serum.
- HBOCs attenuated the release of inflammatory cytokines, including tumor necrosis factor-α and interleukin-1β, post-CPB.
Conclusions:
- HBOCs demonstrate a potential to reduce cerebral damage associated with cardiopulmonary bypass.
- The neuroprotective effects of HBOCs may be linked to improved tissue oxygen delivery during CPB.
Abstract:
In order to investigate whether hemoglobin-based oxygen carrier (HBOC) attenuates cardiopulmonary bypass (CPB)-induced cerebral damage. Male adult Beagle dogs were randomly divided into sham, control, and HBOC groups. After establishment of CPB model, hearts were arrested for 2 h and reperfused for 2 h. HBOC improved intracerebral O2 tensions and reduced the releases of biomarkers for cerebral damage, including neuron-specific enolase and S100β in both cerebrospinal fluid and serum. Moreover, HBOC attenuated the releases of tumor necrosis factor-α and interleukin-1β after CPB. Therefore, our findings suggest that HBOC could reduce cerebral damage after CPB, which was probably associated with improvement of tissue O2 preload.
