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Pulmonary hypertension in patients with COPD: NO treatment?
  1. J Pepke-Zaba,
  2. N W Morrell
  1. Pulmonary Vascular Diseases Unit, Papworth Hospital, Papworth Everard, Cambridgeshire CB3 8RE, UK
  1. Correspondence to:
    Dr N W Morrell, Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Box 157, Hills Road, Cambridge CB2 2QQ, UK;
    nwm23{at}cam.ac.uk

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The application of “pulsed” NO combined with LTOT may have a role in treating pulmonary hypertension secondary to COPD.

Following the identification of nitric oxide (NO) in 1986 as “endothelium derived relaxing factor”, there has been an exponential growth in our understanding of the physiological role of NO culminating in the award of a Nobel Prize, and the naming of NO as “molecule of the decade”.1 Considerable research has subsequently been devoted to understanding the role of this molecule in vascular biology in general, and the pulmonary vascular system in particular.

NO is an unstable radical with a low blood gas partition coefficient. For decades NO was considered an environmental contaminant produced by bacteria and internal combustion engines. Believed to be highly toxic, it appeared an unlikely candidate for a major role as a biological mediator. However, within the last 15 years it has become clear that endogenously produced NO is ubiquitous in mammalian systems, playing an important role in both health and disease: in the regulation of blood pressure and flow, inflammatory responses, and neurotransmission. Insight into these physiological roles has led to its use as a therapeutic agent in a number of clinical settings.

There are ample data to support a major role for NO in the regulation of tone and vascular remodelling in the normal and diseased pulmonary circulation. Endothelial NO contributes significantly to the normally low …

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