Morphometry and myocardial biochemistry 8 weeks after myocardial infarction.

<p>All values are mean ± SD. Comparisons were made by one-way ANOVA with Bonferroni’s post-hoc test.</p>*<p>denotes p<0.05,</p>**<p>p<0.01,</p>***<p>p<0.001 vs group S and ^#p<0.05,</p>###<p>p<0.001 vs group MI.</p

Left ventricular morphology and function derived from MRI 8 weeks post myocardial infarction.

<p>Group S are untreated wild-type sham-operated mice; Group MI are untreated wild-type infarcted mice; Group MI+R are wild-type infarcted mice treated with ribose; Group MI+C+R are infarcted creatine transporter overexpressing mice treated with ribose. Infarcted groups were matched for infarct size (A). Left ventricular remodelling and function was measured by cine-MRI (B–F). Data are reported as mean ± SD. *** denotes p<0.001 (1-way ANOVA with Bonferroni’s correction).</p

Oral ribose treatment increases ribose-5-phosphate levels in the heart.

<p>Myocardial ribose-5-phosphate levels following administration of ribose (10% w/v) in drinking water for seven weeks. Control n = 5, ribose n = 4, mean ± SD, ** denotes p<0.01.</p

Factors influencing ejection fraction by correlation analysis.

<p>Ejection fraction assessed by MRI 8 weeks after myocardial infarction correlated well with infarct size (A), but not with myocardial total adenine nucleotides (B), or myocardial creatine levels (C). Correlation analysis and linear regression is for all groups analysed together. Group MI are untreated wild-type infarcted mice; Group MI+R are wild-type infarcted mice treated with ribose; Group MI+C+R are infarcted creatine transporter overexpressing mice treated with ribose.</p

Left ventricular haemodynamic parameters 8 weeks post myocardial infarction.

<p>Group S are untreated wild-type sham-operated mice; Group MI are untreated wild-type infarcted mice; Group MI+R are wild-type infarcted mice treated with ribose; Group MI+C+R are infarcted creatine transporter overexpressing mice treated with ribose. Heart rate (A), LV end-systolic and end-diastolic pressures (B–C) and maximal and minimal rates of pressure change (D–E) under baseline non-stimulated conditions. Differences analysed by one-way ANOVA with Bonferroni’s correction. ** denotes p<0.01 and *** p<0.001 versus group S. There was no difference between any of the infarcted groups. Panels F–H show heart rate and maximal and minimal rates of pressure change before and after stimulation with dobutamine (16 ng/g BW/min). Effect of genotype and dobutamine assessed by two-way ANOVA with post-hoc Bonferroni’s correction. ^ denotes p<0.05, ^^ p<0.01, ^^^ p<0.001 for dobutamine (black bars) vs baseline (white bars) and * denotes p<0.05, ** p<0.01, *** p<0.001 versus sham at the same dobutamine dose. Data are mean ± SD.</p