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Nitric oxide was largely regarded as a toxic pollutant until 1987, when its biologic similarities to endothelium-derived relaxing factor were demonstrated.1 Subsequently, nitric oxide and endothelium-derived relaxing factor were considered a single entity, modulating vascular tone through the stimulated formation of cyclic guanosine 3',5'-monophosphate (Figure 1).2 Endogenous nitric oxide is formed from the semiessential amino acid L-arginine by one of three (neural, inducible, and endothelial) isoforms of nitric oxide synthase. The physiologic role of endogenous nitric oxide was first shown when an infusion of an inhibitor of all forms of nitric oxide synthase in healthy volunteers led to
Chemical Reactions of Inhaled Nitric Oxide
Physiologic Effects of Inhaled Nitric Oxide on the Cardiovascular System
Direct Cytotoxicity and Effects on Inflammation
Other Effects
Administration of Inhaled Nitric Oxide to Adults
Route, Monitoring, and Safety
DoseResponse Relationship
Clinical Indications for Administering Inhaled Nitric Oxide to Adults
Acute Lung Injury and the Acute Respiratory Distress Syndrome
Targeting Pulmonary Vascular Resistance
Lung Transplantation
Sickle Cell Disease
Alternatives and Adjuncts to Inhaled Nitric Oxide
Other Inhaled Vasodilators
Adjunctive Therapies That Increase the Effectiveness of Inhaled Nitric Oxide
Conclusions and Future Directions
Source Information
From the Adult Intensive Care Unit and Intensive Care Services, Royal Brompton Hospital, and Imperial College London both in London.
Address reprint requests to Dr. Evans at the Unit of Critical Care, Imperial College London, Royal Brompton Hospital, Sydney St., London SW3 6NP, United Kingdom, or at t.evans@rbh.nthames.nhs.uk.
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