Neutrophil-derived, oxygen free radical-mediated cardiovascular dysfunction

Area of Science:

• Cardiovascular Physiology
• Immunology
• Oxidative Stress

Background:

• Neutrophil-derived oxygen free radicals are suspected contributors to cardiovascular dysfunction in various conditions.
• Previous studies lacked direct evidence linking neutrophil oxygen radicals to cardiovascular impairment.

Purpose of the Study:

• To directly demonstrate that activated neutrophils and their derived oxygen free radicals cause cardiovascular dysfunction in vivo.
• To investigate the role of neutrophil activation in mediating cardiac functional changes.

Main Methods:

• Activation of the canine neutrophil system in vivo.
• Measurement of cardiovascular parameters including mean arterial pressure and cardiac index.
• Assessment of effects following neutrophil depletion or administration of superoxide dismutase and catalase.

Main Results:

• Activated neutrophils in vivo generated oxygen free radicals.
• This generation led to significant decreases in mean arterial pressure and cardiac index.
• No significant effects were observed on the myocardial conduction system.
• Neutrophil depletion or antioxidant treatment (superoxide dismutase and catalase) abolished these cardiovascular effects.

Conclusions:

• Neutrophil-derived reduced oxygen intermediates directly induce severe cardiovascular dysfunction.
• These findings provide direct evidence for the role of neutrophil oxygen radicals in mediating cardiac impairment.