ObjectiveTo evaluate the efficacy and reversible effect of anti-VCAM-1 ultrasound-targeted microbubbles on extracorporeal circulation (ECC) related bone marrow neutrophil releasing. MethodsThirty-six male SD rats were randomly divided into 6 groups with 6 rats in each group, including an antibody group (group A), antibody with ultrasound group (group AU), targeted microbubble group (group T), targeted microbubble rupture group (group TU), post-ECC plasma simulation group (group MC) and control group (group C) after in situ perfusion model establishment. Rats in group C received buffer perfusion for 4 cycles, and rats in other groups received perfusion for 5 cycles. After buffer perfusion for the first cycle, post-ECC plasma was infused to each group from the second cycle to the fifth cycle in group MC, A, AU, T and TU. Rats in group A and AU received injection with anti-VCAM-1 antibodies, while rats in group T and TU were given anti-VCAM-1 targeted microbubbles after the second perfusion cycle. Same ultrasound radiation was given to group AU and TU in the third perfusion cycle. Neutrophil counts from perfusate were compared among the 6 groups. ResultsUnder simulated inflammatory condition after ECC, compared with group MC, significant reduction of neutrophil count released from bone marrow was found in group A and T, especially in group T (P < 0.05). After ultrasonic radiation, neutrophil mobilization recovered in group TU and its neutrophil count was significantly higher than that of group T (P < 0.05). There was no significant difference in neutrophil count between group A and AU in each perfusion cycle (P > 0.05). ConclusionsAnti-VCAM-1 targeted microbubbles can block the binding of VCAM-1 and its ligand, and form a barrier on the surface of bone marrow sinusoids endothelium to inhibit neutrophils migrating and releasing. The binding of VCAM-1 and its ligand on microbubbles is separated by cavitation of disrupting microbubbles with ultrasound, and neutrophils recover the ability to cross the sinusoidal endothelium of bone marrow in inflammatory conditions to achieve the controllability of neutrophil releasing.