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Heparin, urokinase, and ancrod alter neutrophil function
J A Freischlag1, M D Colburn, W J Quiñones-Baldrich
1Section of Vascular Surgery, University of California, School of Medicine, Los Angeles.
Journal of Vascular Surgery
|October 1, 1992
Summary
Heparin, urokinase, and ancrod significantly inhibit neutrophil (polymorphonuclear neutrophils [PMNs]) chemotaxis, a key factor in reperfusion injury. These common antithrombotic agents did not affect PMN superoxide anion production.
Area of Science:
- Immunology
- Pharmacology
- Cardiovascular Research
Background:
- Neutrophils, or polymorphonuclear neutrophils (PMNs), are implicated in mediating reperfusion injury.
- Heparin, urokinase, and ancrod are widely used antithrombotic agents.
- The effects of these agents on PMN function remain largely unknown.
Purpose of the Study:
- To investigate the effects of heparin, urokinase, and ancrod on human PMN function.
- To determine if these agents impact superoxide anion production, chemotaxis, or phagocytosis.
Main Methods:
- Human PMNs were incubated with varying concentrations of heparin, urokinase, or ancrod.
- Superoxide anion production was measured via spectrophotometric assay.
- PMN chemotaxis and phagocytosis were assessed using a Neuro Probe chamber and opsonized zymosan particles, respectively.
Main Results:
- None of the tested agents significantly altered superoxide anion production by PMNs at any concentration.
- All three agents (heparin, urokinase, and ancrod) demonstrated significant inhibition of PMN chemotaxis (p < 0.01).
- The control group showed an average of 27.6 +/- 4.9 PMNs.
Conclusions:
- Heparin, urokinase, and ancrod do not affect PMN superoxide anion production.
- These antithrombotic agents significantly impair PMN chemotaxis.
- The findings suggest a potential role for these agents in modulating inflammatory responses associated with reperfusion injury.