Inflammatory effects of blood-air interface in a porcine cardiopulmonary bypass model

Benjamin D. Carr, Thomas J. Johnson, Amalia Gomez-Rexrode, Azmath Mohammed, Megan Coughlin, John M. Toomasian, Alvaro Rojas-Pena, Robert H. Bartlett, Jonathan W. Haft

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)72-78
Number of pages7
JournalASAIO Journal
Volume66
Issue number1
DOIs
StatePublished - Jan 1 2020

Bibliographical note

Funding Information:
Supported by NIH R21 HL125961-01A1, and in part by the University of Michigan Undergraduate Research Opportunity Program (UROP).

Keywords

  • CD11b
  • CPB
  • SIRS
  • blood activation
  • blood trauma
  • cardiopulmonary bypass
  • cardiotomy suction
  • inflammation
  • leukocyte activation
  • platelet activation
  • systemic inflammatory response

PubMed: MeSH publication types

  • Journal Article
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

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