Effects of endotoxin on regulation of intestinal smooth muscle nitric oxide synthase and intestinal transit

Joseph J. Cullen, David Mercer, Marilyn Hinkhouse, Kimberly S. Ephgrave, Jeffrey L. Conklin

Research output: Contribution to journalArticlepeer-review

39 Scopus citations


Background. The disrupted intestinal transit during endotoxemia may be mediated by nitric oxide (NO). We hypothesized that the isoforms of nitric oxide synthase (NOS) are up-regulated in intestinal smooth muscle during endotoxemia and that the scavenging of NO will normalize transit. Methods. Rats were given Escherichia coli lipopolysaccharide (LPS) 10 mg/kg intravenously and were killed 4 hours later. To determine the activity of NOS isoforms in the jejunum and ileum, the conversion of tritiated L-arginine to tritiated L-citrulline was measured. Western immunoblots were performed by incubating the extracted protein with specific polyclonal antibodies. To determine intestinal transit, rats were divided into 4 groups: 0.9% sodium chloride 1 mL/h intravenously for 5 hours, LPS 10 mg/kg intravenous bolus plus 1 mL/h 0.9% sodium chloride intravenously, LPS plus oxyhemoglobin 0.5 g/kg/h intravenously, and oxyhemoglobin 0.5 g/kg/h intravenously. Results. LPS increased the constitutive and inducible NOS enzyme activities in the jejunum and ileum. Western blots demonstrated that LPS up-regulates both the NOS1 and NOS2 isoforms in jejunal and ileal smooth muscle. Oxyhemoglobin alone increased intestinal transit compared with controls, whereas endotoxemia increased intestinal transit, which was ameliorated with infusions of oxyhemoglobin. Conclusions. NO may play a major role in mediating the rapid intestinal transit induced by endotoxemia.

Original languageEnglish (US)
Pages (from-to)339-344
Number of pages6
Issue number3
StatePublished - 1999
Externally publishedYes

ASJC Scopus subject areas

  • Surgery


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