Selective inhibition of inducible nitric oxide in ischemia-reperfusion of rat small intestine

Ji Chang Chen, Han Ming Chen*, Ming Hwang Shyr, Ling Ling Fan, Tsu Yuan Chi, Chung Pi Chi, Miin Fu Chen

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

27 Scopus citations


Purpose: We investigated the role of constitutive and inducible nitric oxide (NO) synthases in intestinal ischemia-reperfusion (I/R) injury by observing the alterations in hemodynamics and intestinal microcirculation in response to I/R in rats, with or without inhibitors of NO synthases. Methods: Adult male Sprague-Dawley rats (n = 9/group) received a standard I/R procedure alone: I/R plus intravenous administration of aminoguanidine (an inhibitor of inducible NO synthase); I/R plus L-NAME (N(G)-nitro-L-arginine methyl ester, an inhibitor of constitutive and inducible NO synthase); IR + L-Arg (L-arginine, an NO precursor); or a sham operation plus the vehicle. The I/R procedure was performed by clamping the perfusion vessels of a segment of the terminal ileum, and medication was administered intravenously before and after intestinal ischemia. The intestinal perfusion and leukocyte- endothelial interactions were evaluated with in vivo microscopy and laser Doppler flowmetry. Surface expression of CD11b (an adhesion molecule) of circulating granulocytes was measured with flow cytometry. Results: Intestinal I/R produced circulatory, alterations, intestinal microcirculatory, derangement, energy depletion, and lipid peroxidation. Aminoguanidine significantly attenuated the reperfusion-related depression of mean arterial pressure (MAP), the decrease in intestinal perfusion index, the decrease in tissue ATP preservation, the increase in tissue malondialdehyde (MDA) level, and the expression of CD11b of circulating granulocytes. Administration of L-NAME had only minor and transient effects on reperfusion- related changes of MAP, intestinal flux, numbers of adherent leukocytes, and CD11b expression, but had some protective effects on tissue MDA and adenosine triphosphate levels and flow velocity. L-Arg further decreased the MAP but did not affect reperfusion-related variables. Conclusions: Our results show that the selective inhibition of inducible NO synthase by aminoguanidine attenuates the hemodynamic and microcirculatory derangement that results from intestinal I/R.

Original languageEnglish
Pages (from-to)213-218
Number of pages6
JournalJournal of the Formosan Medical Association
Issue number3
StatePublished - 03 2000


  • Adhesion
  • Aminoguanidine
  • CD11b
  • Ischemia-reperfusion
  • L-arginine
  • Microcirculation
  • N(G)-nitro-L-arginine methyl ester
  • Nitric oxide


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