You are here

Article Text

Article menu
Letters to the editor
Excess nitric oxide in ulcerative colitis may be generated by nitric oxide synthase independent pathways
  1. Z ZHANG,
  2. D P NAUGHTON,
  3. E CARTY,
  4. D S RAMPTON
  1. MRC Collaborative Centre,
  2. 1–3 Burtonhole Lane,
  3. Mill Hill, London NW7 1AD, UK and
  4. Inflammation Research Group and
  5. Digestive Diseases Research Centre,
  6. St Bartholomew’s and Royal London
  7. School of Medicine and Dentistry,
  8. London E1 2AD, UK

https://doi.org/10.1136/gut.44.3.439-d

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    Editor,—Kimura et al(Gut1998;42:180–7) provide further data in support of the proposal that production of nitric oxide (NO) in ulcerative colitis (UC) is ascribable primarily to the action of inducible NO synthase (NOS) on l-arginine.1-3

    This reaction relies on molecular oxygen as a substrate (fig1).4 However, the Po 2 of gas in the normal colon is low (sometimes only 1–2 mm Hg), not only as a result of bacterial utilisation of oxygen, but also reflecting mucosal hypoxia as a result of cellular metabolism and counter current diffusion of oxygen between mucosal capillaries.5 In active UC, mucosal ischaemia and conversion of oxygen to reactive oxygen …

    View Full Text