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Human neutrophil degranulation during extracorporeal circulation.
Blood
|January 1, 1987
Summary
Cardiopulmonary bypass activates neutrophils, releasing lactoferrin and elastase. Prostaglandin E1 and lidocaine show potential in inhibiting these harmful inflammatory responses during extracorporeal circulation.
Area of Science:
- Biomedical Engineering
- Cardiovascular Surgery
- Hematology
Background:
- Cardiopulmonary bypass (CPB) can lead to hemostatic failure and pulmonary dysfunction.
- Blood contact with synthetic surfaces during CPB activates platelets and leukocytes.
- Neutrophil activation is implicated in CPB-induced complications.
Purpose of the Study:
- To investigate neutrophil activation mechanisms during simulated extracorporeal circulation.
- To document neutrophil lactoferrin and elastase release during clinical CPB.
- To evaluate the inhibitory effects of prostaglandin E1 (PGE1) and lidocaine on neutrophil activation markers.
Main Methods:
- Simulated in vitro extracorporeal circulation using an oxygenator bypass circuit.
- Analysis of plasma markers: beta-thromboglobulin (beta TG), lactoferrin, and neutrophil elastase.
- Administration of PGE1 and lidocaine during simulated and clinical CPB to assess inhibition.
Main Results:
- Clinical CPB showed decreased platelet counts and increased plasma beta TG.
- Neutrophil counts initially decreased then rose; plasma lactoferrin and elastase significantly increased.
- In vitro studies demonstrated increased beta TG, lactoferrin, and elastase; lidocaine inhibited elastase release, while PGE1 inhibited beta TG and elastase release.
Conclusions:
- Neutrophil activation and release of specific proteins occur during CPB.
- Lidocaine and PGE1 exhibit differential inhibitory effects on neutrophil activation markers.
- These findings suggest distinct pathways for neutrophil protein release, potentially targetable for mitigating CPB-related complications.