Fulltext

Nitric Oxide and Infection: Another View

Schoedon, G. ; Schneemann, M. ; Walter, R. ; Blan, N. ; Hofer, S. ; Schaffner, A.

In: Clinical Infectious Diseases, 1995, vol. 21, no. Supplement_2, p. S152-S157

Add to personal list
    Title
    • Nitric Oxide and Infection: Another View
    Author
    • Schoedon, G.. From the Division of Infectious Diseases, Clinical Mycology Laboratory, Department of Medicine, University of Zürich Medical School, Zürich, Switzerland
    • Schneemann, M.. From the Division of Infectious Diseases, Clinical Mycology Laboratory, Department of Medicine, University of Zürich Medical School, Zürich, Switzerland
    • Walter, R.. From the Division of Infectious Diseases, Clinical Mycology Laboratory, Department of Medicine, University of Zürich Medical School, Zürich, Switzerland
    • Blan, N.. From the Division of Infectious Diseases, Clinical Mycology Laboratory, Department of Medicine, University of Zürich Medical School, Zürich, Switzerland
    • Hofer, S.. From the Division of Infectious Diseases, Clinical Mycology Laboratory, Department of Medicine, University of Zürich Medical School, Zürich, Switzerland
    • Schaffner, A.. From the Division of Infectious Diseases, Clinical Mycology Laboratory, Department of Medicine, University of Zürich Medical School, Zürich, Switzerland
    Document Type
    • Postprint
    Classification
    • Health
    OAI-PMH Identifier
    • oai:doc.rero.ch:290243
    Summary
    Nitric oxide (NO) has been nicknamed "murderer” and "mediator” because it has toxic and signaling properties. We review these two aspects of NO synthesis from the perspective of the clinical infectious disease specialist by considering the potential of NO as an endothelium-derived relaxing factor (EDRF) in inflammation and sepsis and its potential as an antimicrobial system. We deviate from observations in recent authoritative reviews and point to important speciesdifferences that make it unlikely that NO serves as an EDRF mediating inflammatory vasodilatation in humans or that NO synthesized by human phagocytes has an antimicrobial function.We propose that in humans, NOsynthesis is moreconfined and compartmentalized than in certain other animal species, and therefore, unwelcome toxicity, vasodilatation, or disturbance of paracrine signaling mechanisms (i.e., modulation of phagocytic cell functions) are avoided during inflammation