Abstract

Gazeous nitric oxide (NO) and nitrogen dioxide (NO2) are well known atmospheric outdoor pollutants which toxicity was extensively studied in the seventies. In the eighties, inhaled NO was used in humans as an alternative to CO to measure the oxygen diffusing capacity of the lungs [1, 2]. In 1987, one of the endothelium-derived relaxing factors [3] was identified as NO [4]. It was then demonstrated that NO was continuously released by the endothelial cells after activation of the constitutive NO synthase in response to shear stress. Later, NO was found to be involved in a large number of physiological systems [5, 6] such as coagulation [7, 8], neuronal transmission and inflammation.KeywordsNitric OxidePulmonary HypertensionPulmonary Arterial HypertensionAcute Respiratory FailureAdult Respiratory Distress SyndromeThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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