Active abdominal compression-decompression cardiopulmonary resuscitation attenuates neuroinflammation associated with TLR4/NF-κB signaling in a rat model of cardiac arrest.

Cardiac arrest (CA) induces cerebral ischemia-reperfusion injury, which is a major contributor to mortality and neurological dysfunction following resuscitation. Active abdominal compression-decompression cardiopulmonary resuscitation (AACD-CPR) has emerged as a potential alternative to standard cardiopulmonary resuscitation (STD-CPR). The present study aimed to investigate whether AACD-CPR attenuates neuroinflammation after CA/CPR and whether this effect is associated with changes in Toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB)-related signaling. A rat model of CA was established, followed by resuscitation with either STD-CPR or AACD-CPR. Return of spontaneous circulation (ROSC), survival, NDS and neuronal injury were evaluated. The expression levels of TLR4, NF-κB and inflammation-related markers, including tumor necrosis factor-α, interleukin-1 β, glial fibrillary acidic protein (GFAP) and ionized calcium-binding adapter molecule 1 in brain tissue were assessed by western blotting and immunohistochemistry. Compared with STD-CPR, AACD-CPR markedly reduced resuscitation duration and improved early neurological outcomes. Although the ROSC rate and short-term survival rate were numerically higher in the AACD-CPR group than in the STD-CPR group, these differences did not reach statistical significance and therefore should not be interpreted as evidence of a definitive survival benefit. AACD-CPR was also associated with reduced neuronal injury, decreased expression of proinflammatory cytokines and glial activation markers and downregulation of TLR4/NF-κB-related proteins in brain tissue. AACD-CPR improved early neurological outcomes and attenuated neuroinflammatory responses in this rat model of CA/CPR. These effects were accompanied by suppression of TLR4/NF-κB-related signaling. However, as this was a preclinical small-animal study, the findings should be interpreted cautiously and not as evidence that AACD-CPR can clinically replace STD-CPR. Further studies in large-animal models and well-designed clinical investigations are required to validate its safety, feasibility and translational relevance.