Superoxide, NO and CO in liver microcirculation: Physiology and pathophysiology

Makoto Suematsu, Yusuke Kumamoto, Tsuyoshi Sano, Yoshiyuki Wakabayashi, Yuzuru Ishimura

Research output: Contribution to journalArticlepeer-review


Superoxide anion (O2-), nitric oxide (NO), and carbon monoxide (CO) are metabolites of molecular oxygen endogenously generated through oxygen activation by a variety of oxidases and oxygenases such as xanthine oxidase and NADPH oxidase, NO synthase, and heme oxygenase, respectively. There is an increasing body of evidence showing that these active oxygen metabolites not only exert their cytotoxic properties but also play a modulatory role in regulation of cell function in and around hepatic sinusoidal vessels. Among them, CO generated by heme oxygenase is a novel vasodilatory mediator which can upregulate cGMP in fat-storing Ito cells, liver-specific microvascular pericytes which encircle sinusoidal walls, and thereby control the microvascular tone under control conditions. When exposed to endotoxemia, Kupffer cells and hepatocytes can express inducible NO synthase activity which serves as a NO-dependent cytotoxic mechanisms involving peroxynitrite formation. Disclosure of the whole picture of NO- and CO-dependent mechanisms for regulation of hepatic microcirculation gives a clue to understanding the physiology and pathophysiology of liver function.

Original languageEnglish
Pages (from-to)154-160
Number of pages7
JournalJournal of Hepato-Biliary-Pancreatic Surgery
Issue number2
Publication statusPublished - 1996 Jan 1


  • Carbon monoxide
  • Ito cells
  • Nitric oxide
  • Oxidative stress
  • Sinusoids

ASJC Scopus subject areas

  • Surgery
  • Hepatology


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