(A) Rate pressure product (RPP), as a percentage of pre-ischaemic levels, following 32 min of 0.3 ml.min-1gww-1 low-flow ischaemia, with or without delivery of 2.5 µM of the β-hydroxy-β-methylglutaryl (HMG)-CoA synthase (HMGCS) inhibitor hymeglusin in the perfusion buffer (two groups, n = 5 hearts each). (B) Respiration rates corrected for wet mass. Malate and octanoyl carnitine were added initially to stimulate leak respiration, then, sequentially, adenosine diphosphate (ADP) to stimulate β-oxidation-supported OXPHOS, pyruvate, and glutamate to support electron flux through complex I, succinate to additionally support electron flux through complex II, and finally rotenone to inhibit complex I- and isolate complex II-supported respiration. The non-ischaemic control group consisted of n = 5 hearts perfused aerobically for 96 min. The I/R control and I/R hymeglusin groups consisted of n = 5 hearts per group subjected to 32 min of aerobic perfusion at 100 mmHg, 32 min of 0.3 ml.min-1gww-1 low-flow ischaemia, then 32 min of aerobic reperfusion at 100 mmHg, with either vehicle or 2.5 µM hymeglusin administered in the perfusion buffer. Results are presented as mean ± SEM. *p<0.05, **p<0.01, relative to ischaemic control. †p<0.05, #p<0.01, and ‡‡‡p<0.001, relative to non-ischaemic control.