Volume 3 Supplement 1

19th International Symposium on Intensive Care and Emergency Medicine

Open Access

Jejunal mucosal NO production and substrate dependency during mesenteric hypoperfusion in pigs

  • J Snygg1,
  • A Åneman1,
  • A Pettersson1 and
  • I Fändriks1
Critical Care20003(Suppl 1):P167


Published: 16 March 2000

Background and aims

Intestinal NO production has been attributed a central role in the maintenance of the intestinal mucosal barrier. Hypofunction of this barrier has been suggested to be one important factor behind the initiation of the multiple organ dysfunction syndrome. Jejunal NO formation, as we previously have reported, has been shown to be impaired during mucosal hypoperfusion [1]. This study was undertaken to investigate if the impaired jejunal NO levels could be due to restricted mucosal availability of NO-synthase substrates, i.e. oxygen and/or L-arginine.


Chloralose-anesthetized pigs (n = 18) were prepared for jejunal intraluminal perfusion with 150 mM NaCl or 3 mM L-arginine solution and then subjected to cardiac tamponade. Jejunal mucosal NO formation was measured with a tonometric technique. Mesenteric blood flow was measured as portal blood flow and mucosal perfusion was measured by laserdoppler flowmetry. Regional oxygen consumption was calculated from blood samples.


Cardiac tamponade reduced jejunal NO formation (-52%), mesenteric oxygen delivery (-75%), oxygen consumption (-39%) and mucosal laser doppler flow (-43%). Oxygenation of the jejunal intraluminal perfusate completely restored the intestinal NO levels within 30 min. Presence of L-arginine was without effect.


The study indicates that oxygen rather than L-arginine is the rate limiting factor for mucosal NO production during reduced splanchnic perfusion.

Authors’ Affiliations

Department of Anaesthesiology and Intensive Care, Sahlgrens University Hospital Eastern hospital


  1. Åneman A, Snygg J, Pettersson A, Johansson B, Holm M, Fändriks L: Detecting gastrointestinal hypoperfusion during cardiac tamponade in pigs: A role for nitric oxide tonometry? Crit Care Med 1998, 26: 1251. 10.1097/00003246-199807000-00030View ArticlePubMedGoogle Scholar


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