Abstract
The gas nitric oxide (NO) has attracted increased interest since 1987 when Palmer et al. [1], Furchgott [2] and Ignarro et al. [3] independently described that the elusive endothelium-derived relaxing factor (EDRF) was indistinguishable from NO. NO activates guanylate cyclase which in turn increases cGMP in smooth muscle cells, causing relaxation [4]. Hemoglobin antagonizes the vasodilatory properties of NO by binding NO extracellularly to heme [5]. In 1988, Higenbottam et al. [6] claimed selective pulmonary vasodilation in patients with endstage pulmonary hypertension by administering NO as a component of inhaled gas. A dose-response curve was not reported, and the observed dilatation was minimal.
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References
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© 1992 Springer-Verlag Berlin Heidelberg
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Frostell, C.G. (1992). Effects of Inhaled Nitric Oxide in Volunteers. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1992. Yearbook of Intensive Care and Emergency Medicine, vol 1992. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84734-9_22
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DOI: https://doi.org/10.1007/978-3-642-84734-9_22
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