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. Author manuscript; available in PMC: 2009 May 20.
Published in final edited form as: Circulation. 2008 May 12;117(20):2626–2636. doi: 10.1161/CIRCULATIONAHA.107.737031

Figure 4.

Figure 4

a) BH4 reversed myocardial oxidant stress. Example of DHE fluorescence images show increased ROS at 4 and 9 wks TAC that is reversed with BH4 therapy. Summary data are to the right. b) Lucigenin chemilumenescence (CL) assay confirms a marked rise in O2− at 9 wks TAC that is reversed to control levels by BH4 treatment. c) Left: BH4 and Tempol have similar dose-dependent anti-oxidant effects in vitro. Assay used xanthine/xanthine oxidase O2− generator system. Right: O2−generation in myocardium of 9-wks TAC is reduced by delayed Tempol treatment, similar to that with BH4 (panel d). d) Tempol does not reduce LV mass, but ejection fraction borderline increased (p=0.08). (*:p<0.001 vs 9 wks TAC, †: p=0.08 vs TAC-untreated). c) Tempol does not reduce TAC-stimulated fibrosis, and more modestly reduces myocyte size compared to BH4 (p<0.0001). Upper panels are stained with Masson-trichrome, bottom with H/E. e) Tempol does not reverse eNOS uncoupling reflected in dimer/monomer ratios on immunoblot.