Related Experiment Video
Updated: Aug 13, 2026
Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
Published on: April 6, 2017
Possible Clinical Effects of Polymyxin B-Immobilized Fiber Columns via Platelet-Derived Lipid Mediators: A
Shintaro Suzuki1, Satoshi Kazuma2, Hiroomi Tatsumi1
1Department of Intensive Care Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Introduction:
Endotoxin removal therapy using a polymyxin B-immobilized fiber column (PMX) has been reported to improve hemodynamics in patients with septic shock. However, the mechanisms underlying the blood pressure-increasing effects of PMX treatment remain unclear, and factors other than endotoxin adsorption may be involved. This study focused on vasoconstrictive lipid mediators in the blood and comprehensively analyzed these mediators in patients with septic shock.
Methods:
This prospective observational study included 10 patients with septic shock who underwent PMX treatment. Blood samples were collected at multiple time points up to 120 min after PMX initiation, and 23 lipid mediators were measured by mass spectrometry. Hemodynamic changes were evaluated using the vasopressor dependency index (VDI). Furthermore, platelet-rich plasma from healthy subjects was incubated with PMX fibers in vitro to assess platelet adhesion by electron microscopy and thromboxane production.
Results:
Among the 10 patients included, the plasma concentration of thromboxane B2 (TXB2), a stable derivative of thromboxane A2 (TXA2), was significantly higher at the PMX column outlet than at the inlet. This difference in TXB2 concentration showed a significant positive correlation with platelet count. Patients with higher platelet counts tended to exhibit a greater decrease in VDI, although the difference was not statistically significant. In vitro experiments demonstrated that platelets adhered to PMX fibers, accompanied by morphological changes, and that the fibers stimulated TXB2 production. Importantly, this production was suppressed by an antibody against the platelet surface antigen αIIbβ3.
Conclusion:
TXA2, produced by platelets upon contact with PMX fibers during treatment, may contribute to the rapid increase in blood pressure observed after initiation of therapy.
Insights
Polymyxin B-immobilized fiber (PMX) therapy for septic shock may increase blood pressure by stimulating platelets. Contact with PMX fibers causes platelets to produce thromboxane A2 (TXA2), a vasoconstrictor.
Area of Science:
- Critical care medicine
- Nephrology
- Cardiovascular research
Background:
- Polymyxin B-immobilized fiber (PMX) column therapy improves hemodynamics in septic shock.
- Mechanisms behind PMX-induced blood pressure increase are not fully understood.
- Factors beyond endotoxin adsorption may influence PMX efficacy.
Purpose of the Study:
- To investigate the role of vasoconstrictive lipid mediators in septic shock patients undergoing PMX therapy.
- To analyze changes in lipid mediators and their correlation with hemodynamic parameters.
- To explore the interaction between platelets and PMX fibers in vitro.
Main Methods:
- Prospective observational study of 10 septic shock patients treated with PMX.
- Mass spectrometry analysis of 23 lipid mediators in blood samples.
- In vitro experiments assessing platelet adhesion and thromboxane production on PMX fibers.
Main Results:
- Plasma thromboxane B2 (TXB2) levels were higher post-PMX column, correlating with platelet count.
- Platelets adhered to PMX fibers, exhibiting morphological changes and stimulating TXB2 production.
- PMX-induced TXB2 production was inhibited by an antibody targeting αIIbβ3.
Conclusions:
- Thromboxane A2 (TXA2), generated by platelets interacting with PMX fibers, may contribute to the rapid blood pressure increase during therapy.
- Platelet activation and subsequent TXA2 release are potential mechanisms of PMX treatment in septic shock.