Cardiopulmonary bypass (CPB) causes a systemic inflammatory response syndrome (SIRS) associated with multiorgan injury. A model was developed to test whether a blood–air interface (BAI) in the CPB circuit causes blood element activation and inflammation. Ten healthy swine were placed on partial CPB for 2 hours via the cervical vessels and monitored for 96 hours postoperatively. Five pigs (control group) had minimal air exposure in the circuit, while five were exposed to a BAI simulating cardiotomy suction. There were no significant differences in bypass flow or hemodynamics between the groups. In the BAI group, there was an increase in hemolysis after bypass (plasma-free hemoglobin 5.27 ± 1.2 vs. 0.94 ± 0.8 mg/dl; p = 0.01), more aggressive platelet consumption (28% vs. 83% of baseline; p = 0.009), leukocyte consumption (71% vs. 107% of baseline; p = 0.02), and increased granulocyte CD11b expression (409% vs. 106% of baseline; p = 0.009). These data suggest the inflammatory pattern responsible for the CPB-SIRS phenomenon may be driven by blood–air interaction. Future efforts should focus on BAI-associated mechanisms for minimizing blood trauma and inflammation during CPB.
From the *Extracorporeal Life Support Laboratory, Department of Surgery, Michigan Medicine, University of Michigan, Ann Arbor, Michigan
†Department of Cardiac Surgery, Michigan Medicine, University of Michigan, Ann Arbor, Michigan.
Submitted for consideration May 2018; accepted for publication in revised form October 2018.
Disclosure: The authors have no conflicts of interest to report.
Supported by NIH R21 HL125961-01A1, and in part by the University of Michigan Undergraduate Research Opportunity Program (UROP).
Correspondence: Alvaro Rojas-Pena, Extracorporeal Life Support Laboratory, Department of Surgery, Michigan Medicine, University of Michigan, B560, MSRB II, SPC5686 1150 West Medical Center Drive, Ann Arbor, MI 48109. Email: firstname.lastname@example.org.