Nitric oxide protects against contrast media-increased pulmonary vascular permeability in rats

Toshiaki Sendo, Yasufumi Kataoka, Yuri Takeda, Wakako Furuta, Ryozo Oishi

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)


RATIONALE AND OBJECTIVES. Nitric oxide (NO) regulation of endothelial function is involved in the development of acute lung injury. The role of NO in contrast media-induced increases in pulmonary vascular permeability was investigated in a rat model. METHODS. Nonionic (iohexol) and ionic (ioxaglate) contrast media were intravenously injected at 1.5 mL/min in rats. Pulmonary vascular permeability was evaluated by measuring the amount of Evans blue dye uptake as a quantitative marker of albumin extravasation in lung tissue. RESULTS. Intravenous injections of contrast media at doses of 4 and 6 g I/kg induced a dose-dependent increase in pulmonary vascular permeability. L-Arginine (an NO synthase substrate) and N(G)-nitro-L-arginine (L-NNA) (an NO synthase inhibitor) prevented and aggravated, respectively, the increase in pulmonary vascular permeability induced by the contrast medium. An aggravating action of L-NNA was confirmed by morphological and histological observations, this action being blocked by L-arginine (300 mg/kg) but not by D-arginine. Isosorbide dinitrate (1-20 mg/kg), an NO donor, had a dose-dependent protective effect on ioxaglate-increased vascular permeability. CONCLUSIONS. Our experimental findings suggest that contrast media at high doses produce pulmonary edema by inhibiting endothelial NO production, and nitrovasodilators protect against this adverse effect in rats.

Original languageEnglish
Pages (from-to)472-478
Number of pages7
JournalInvestigative Radiology
Issue number8
Publication statusPublished - Aug 26 2000
Externally publishedYes


  • Contrast media
  • Isosorbide dinitrate
  • Nitric oxide
  • Pulmonary edema
  • Vascular permeability

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging


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