Table 5.
Experimental studies of cardioprotection via sustained periods of opioid receptor agonism (from 24 h to 14 days)
| Putative selectivity | Agent/duration | Species, tissue | Primary outcome | Effect | Implicated effectors or targets | Study |
|---|---|---|---|---|---|---|
| Non-selective | Morphine (14 days) | Rat, isolated heart | Arrhythmogenesis | Improved | Wong & Lee, 1987 | |
| Morphine (5 days) | Mouse, isolated heart | Infarction (LDH) | Improved | Peart & Gross, 2004a | ||
| Contractility | Improved | PKA, β2-adrenoceptors, Gs | Peart & Gross, 2006 | |||
| Morphine (10 days) | Rat, in situ heart | Infarction (TTC) Arrhythmogenesis | Unaltered Improved | Skrabalova et al., 2012 | ||
| DOR | BW-373U86 (5 days) | Mouse, isolated heart | Contractile recovery | Improved | PI3K (Induction) | Peart et al., 2011 |
| MOR/DOR | Eribis peptide 94 (24 h) | Rat, in situ heart | Infarction (TTC) | Improved | NO, mKATP | Gross et al., 2012b |
| KOR | U50,488H (5 days) | Mouse, isolated heart | Contractile recovery | Unaltered | Peart et al., 2011 |
Shown are effects of sustained opioid receptor agonism (24 h to 14 days) on myocardial outcomes from I–R in experimental models. Agents were applied to rodents and myocardial outcomes subsequently assessed in in situ or ex vivo hearts. Primary outcome include myocardial infarction, contractile recovery and arrhythmogenesis. Also shown are the receptors, signalling elements or effector molecules implicated in protection. BW-373U86, 4-[(R)-[(2S,5R)-2,5-dimethyl-4-prop-2-enylpiperazin-1-yl]-(3-hydroxyphenyl)methyl]-N,N-diethylbenzamide; mKATP, mitochondrial KATP channels.