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Remote pharmacological post-conditioning by intrathecal morphine: cardiac protection from spinal opioid receptor
J Ling Ling1, G T C Wong, L Yao
1Department of Anaesthesiology, University of Hong Kong, Hong Kong.
Background:
Intrathecal morphine pre-conditioning attenuates cardiac ischemia-reperfusion injury via activation of central opioid receptors. We hypothesized that intrathecal morphine also post-conditions the myocardium in the rat.
Methods:
Intrathecal morphine at 0.3 μg/kg (LMPC), 3 μg/kg (MMPC) or 30 μg/kg (HMPC) was administered for 5 min before 120-min reperfusion following 30-min ischemia. Infarct size as a percentage of area at risk (IS/AAR) was determined using triphenyltetrazolium staining. MMPC was repeated following the intrathecal administration of nor BNI, NTD, CTOP, or naloxone methiodide (NM), kappa, delta, mu and non-specific opioid receptor antagonists, respectively. The role of peripheral opioid, adenosine and calcitonin gene-related peptide (CGRP) receptors was examined by the intravenous administration of NM, 8-ρ-sulfophenyl theophylline (8-SPT) and human CGRP fragment (CGRP(8-37)), respectively.
Results:
Morphine post-conditioning at all three doses was cardioprotective (IS/AAR of LMPC=37 ± 4%, MMPC=35 ± 5%, HMPC=32 ± 4%, control=50 ± 5%, P<0.01). The prior administration of opioid receptor antagonists intrathecally, as well as intravenous 8-SPT and CGRP(8-37) receptor antagonists, abolished this effect (nor BNI+MMPC=47 ± 7%, NTD+MMPC=49 ± 7%, CTOP+MMPC=45 ± 9%, NM+MMPC=47 ± 6% 8-SPT+MPC=46 ± 5% & CGRP(8-37)+MPC=53 ± 6%, P=0.63). However, the intravenous administration of NM did not prevent the protective effect (34 ± 4%, P<0.01).
Conclusions:
Intrathecal morphine administration can induce pharmacological cardiac post-conditioning as it involves opioid receptor centrally but non-opioid receptors peripherally.
Insights
Intrathecal morphine post-conditioning protects the heart from ischemia-reperfusion injury in rats. This effect involves central opioid receptors and peripheral non-opioid receptors.
Area of Science:
- Cardiology
- Pharmacology
- Neuroscience
Background:
- Intrathecal morphine pre-conditioning is known to reduce cardiac ischemia-reperfusion injury by activating central opioid receptors.
- This study investigated whether intrathecal morphine could also provide cardioprotection when administered after ischemia (post-conditioning).
Purpose of the Study:
- To determine if intrathecal morphine administration post-ischemia can protect the rat myocardium from ischemia-reperfusion injury.
- To elucidate the receptor mechanisms, both central and peripheral, involved in this cardioprotective effect.
Main Methods:
- Rats were subjected to 30 minutes of ischemia followed by 120 minutes of reperfusion.
- Intrathecal morphine was administered at varying doses (0.3, 3, or 30 μg/kg) before reperfusion.
- Infarct size was assessed, and the roles of central and peripheral opioid receptors, adenosine receptors, and calcitonin gene-related peptide (CGRP) receptors were examined using specific antagonists.
Main Results:
- Intrathecal morphine post-conditioning significantly reduced infarct size at all tested doses compared to controls.
- The cardioprotective effect was abolished by central administration of opioid receptor antagonists (norBNI, NTD, CTOP, NM).
- Peripheral administration of adenosine (8-SPT) and CGRP (CGRP(8-37)) receptor antagonists also abolished the protective effect, while peripheral opioid receptor blockade (NM) did not.
Conclusions:
- Intrathecal morphine administration effectively induces pharmacological cardiac post-conditioning in rats.
- The cardioprotection involves the activation of central opioid receptors.
- Peripheral non-opioid receptors, specifically adenosine and CGRP receptors, are also crucial for this protective effect.
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