Related Experiment Video
Updated: Jul 17, 2026
A Recovery Cardiopulmonary Bypass Model Without Transfusion or Inotropic Agents in Rats
Published on: March 23, 2018
Proteomic, transcriptomic, and metabolic mediators of postcardiopulmonary bypass vasoplegia syndrome
Aubrey Galloway1, Caroline Magro1, Chandra Goparaju1
1Department of Cardiothoracic Surgery, NYU Langone Health, New York, NY.
Objective:
Vasoplegia syndrome (VS) after cardiopulmonary bypass (CPB) is associated with a dysregulated inflammatory response and greater rates of morbidity and mortality, but the molecular pathways involved have been incompletely identified. We used multiplexed proteomic and transcriptomic analyses and targeted biochemical assays to identify the inflammatory and metabolic mediators that characterize post-CPB VS.
Methods:
Sixteen matched pairs of patients with (+) and without (-) VS were analyzed pre-CPB and post-CPB for comparative proteomic and transcriptomic differences, with Gene Ontology pathway enrichment. Circulating nitric oxide (NO) metabolites, acetylcholine (ACh), and choline acetyltransferase levels were measured and correlated with VS.
Results:
Baseline proteomic analysis demonstrated elevated tumor necrosis factor-alpha, interleukin-1R1, and interleukin-17RA in patients who were VS+, with activation of inflammatory cytokine, leukocyte activation, and NO biosynthesis pathways. Analysis of temporal pre-to-post CPB proteomic changes in patients who were VS+ demonstrated post-CPB elevation of IL-17A, CXCL2, and VEGFR/FLT, and decreased immune resolving proteins. Post-CPB comparative proteomic analysis demonstrated differential activation of leukocyte trafficking, T-cell differentiation, interleukin-6, and interleukin-17 pathways in patients who were VS+. Transcriptomic analysis demonstrated post-CPB activation of cellular response to hypoxia, cellular stress response, and decreased response to angiotensin pathways. Circulating NO metabolites, ACh, and choline acetyltransferase levels were elevated pre-CPB in patients who were VS+ and increased further post-CPB. Pre-CPB ACh had a 99% area under the curve correlation with post-CPB VS+.
Conclusions:
We demonstrated increased baseline cardiovascular inflammation in patients identified as VS+, which predisposed them to a dysregulated inflammatory response to CPB, and we identified CPB-induced activation of IL-17-skewed multicytokine inflammatory pathways and endothelial activation as mechanistic mediators of post-CPB VS. Circulating ACh was identified as a potential biomarker.
