Figure 6.

_mtDNA damage repair in CAD microvessels induces NO-mediated FMD. (A) Isolated microvessels from showed higher levels of mtDNA damage in patients with CAD than non-CAD. Quantitative end-point PCR was used to measure the relative amplification of an 8.8 kbp segment and a 221 bp segment of the mitochondrial genome and calculate the relative DNA lesion frequency (N = 10–12). (B) NO-driven FMD was restored in microvessels from subjects with CAD after treatment with Endo III (N = 6–8) but not after (C) treatment with inactive mEndo III (N = 3–5). (D) In vessels from subjects without CAD, Endo III prevented the BIBR 1532-induced switch from NO to pathological H₂O₂ (N = 3–4). (E) Smooth muscle response to papaverine was not altered (N = 4–8). * P < 0.05 A unpaired t-test; B–D 2-way ANOVA RM.