Table 4.
Experimental studies of cardioprotection via i.t. or intracerebral opioid receptor agonists
| Putative selectivity | Agent – delivery | Species, tissue | Primary outcome | Effect | Implicated effectors or targets | Study |
|---|---|---|---|---|---|---|
| Non-selective | Morphine – i.t. | Rat, in situ heart | Infarct (TTC) | Improved | DOR, KOR and MOR | Li, et al., 2009 |
| Improved | Central and peripheral adenosine receptors | Yao, et al., 2011 | ||||
| Improved | ANS, bradykinin and CGRP receptors, KATP, Akt, NOS | Wong et al., 2012b | ||||
| Morphine – intracerebral | Rat, in situ heart | Infarct (TTC) | Improved | DOR, KOR and MOR, cerebral calmodulin, CGRP | Zhang et al., 2011 | |
| MOR | Fentanyl – i.t. | Rat, in situ heart | Infarct (TTC) | Improved | Spinal nNOS | Lu et al., 2014 |
Shown are effects of i.t. or i.c.v. opioid receptor agonists on myocardial outcomes from I–R in experimental models. In all cases agonists were applied prior to the ischaemic insult. The primary outcome in all studies was myocardial infarction. Also shown are the receptors, signalling elements or effector molecules implicated in protection. ANS, autonomic nervous system; nNOS, neuronal NOS; TTC, 2,3,5-triphenyl-2H-tetrazolium chloride staining for infarction.