Rationale and objectives: Contrast media induce adverse effects including edema of the face, glottis, or lung. The endothelial function is maintained by nitric oxide (NO). The present study was designed to elucidate the role of NO in mediating endothelium-related adverse effects of contrast media.
Methods: Human microvascular endothelial cells grown on a Transwell membrane were incubated with iohexol or ioxaglate in the absence or presence of N(G)-monomethyl-L-arginine or sodium nitroprusside. After washing cells, the permeability of sodium fluorescein or Evans blue albumin and the accumulation of NO(2)(-) was examined.
Results: Contrast media (50-150 mgI/mL) dose-dependently increased the permeability coefficient by 30% to 230% and inhibited the formation of NO(2)(-) by 40% to 80%. Sodium nitroprusside and N(G)-monomethyl-L-arginine produced protective and aggravating effects on contrast media-increased permeability, respectively.
Conclusions: The present study suggested that contrast media increase vascular endothelial permeability by inhibiting NO production, leading to vascular endothelium-related adverse effects of contrast media.