Table 1.
Effect of hypercholesterolaemia (HC) on cardioprotection induced by ischaemic and pharmacological PC
| Experimental model | Effect on PC | Proposed mechanism(s) | Reference |
|---|---|---|---|
| Isolated rat hearts subjected to PC | Elimination of infarct size reduction by PC | HC abolished PC‐induced inhibition of myocardial MMP2 activation and release | Giricz et al., 2009 |
| Isolated rat hearts subjected to PC | Elimination of infarct size reduction by PC | Loss of cardioprotection by PC in HC is associated with a redistribution of both sarcolemmal and mitochondrial connexin 43 | Görbe et al., 2011 |
| Rats exposed to pacing‐induced PC | Elimination of pacing‐induced cardioprotection by PC | HC induced deterioration of cardiac NO metabolism | Ferdinandy et al., 1997 |
| Rats subjected to three cycles of PC | Elimination of infarct size reduction by PC | HC elevated ADMA and eliminated the cardioprotective effects of PC | Landim et al., 2013 |
| Rabbits exposed to pacing‐induced PC | Elimination of pacing‐induced cardioprotection by PC | HC impaired cardiac NO synthesis | Szilvassy et al., 1995; Ferdinandy et al., 1998a,b |
| Rabbits subjected to one cycle PC | Elimination of the infarct size‐limiting effect of PC | HC prevented ecto‐5′‐nucleotidase activation by PC | Ueda et al., 1999 |
| Rabbits subjected to one cycle of PC | Myocardial infarction reduction by PC was not attenuated by HC | Observational study | Kremastinos et al., 2000 |
| Rabbits subjected to two cycles of PC | Myocardial infarction reduction by PC was not attenuated by HC | Observational study | Iliodromitis et al., 2006 |
| Rabbits subjected to one cycle of PC | Myocardial infarction reduction by PC was not attenuated by HC | Reduced calcium‐ionophore stimulated endothelial NO‐release were found in isolated aortic rings of hypercholesterolemic animals suggesting that NO produced by the endothelium is not a prime factor in the cardioprotective mechanism of PC | Jung et al., 2000 |
| Rabbits subjected to late PC | Elimination of infarct size reduction by late PC | Impaired up‐regulation of BH4, which is essential for inducible nitric oxide (NO) synthase | Tang et al., 2005 |
| Sevoflurane‐induced PC in rats | Elimination of sevoflurane‐induced cardioprotection | HC alterated the upstream signalling of GSK3β | Ma et al., 2013 |
| Sevoflurane‐induced PC in rats | Elimination of sevoflurane‐induced cardioprotection | Interference with the iNOS/mitochondrial ATP‐dependent K+ channel pathway | Zhang et al., 2012 |
| Fasudil induced pharmacological PC in rats | Low‐dose fasudil‐induced PC is abolished by HC, but only high‐dose restored the cardioprotection | Fasudil up‐regulated the PI3K/Akt/eNOS pathway and induced the opening of the mito‐KATP channel | Wu et al., 2014b |
| NO donors induced late PC in rabbits | Hypercholesterolaemia blunted NO donor (diethylenetriamine/NO) ‐induced late PC | Disruption of biochemical pathways distal to the generation of NO | Tang et al., 2004 |