FIG. 5.

Effect of captopril on HBOC-induced endothelial dysfunction is ROS- and NAD(P)H oxidase dependent. (A, E) Representative immunohistochemical staining of coronary arteries for DHE and vWF. Scale bar: 200 μm. (B–D) The ROS production, SOD activity, and MDA formation in HUVECs after indicated treatment. One unit of SOD activity corresponded to 50% reduction of absorbance at 550 nm. (F–I) SNP-induced endothelium-independent relaxation and ACh-induced endothelium-dependent relaxation in coronary arteries after indicated treatment. Control vessels were incubated with KH solution alone. (J–L) ROS production, SOD activity, and MDA formation in HUVECs after indicated pretreatment and exposure to the 3%HBOC. Values are presented as mean±SD (n=5 to 6 per group). *p<0.05 and **p<0.01 versus the 0.1%HBOC group; ^#p<0.05 and ^##p<0.01 versus the 3%HBOC group. ACEI in the figure indicates ACE inhibitor captopril. ACE, angiotensin-converting enzyme; DHE, dihydroethidium; MDA, malonaldehyde; ROS, reactive oxygen species; SOD, superoxide dismutase; vWF, von Willebrand factor. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars