Exogenous activation of δ- and κ-opioid receptors affords cardioprotection in isolated murine heart.
Author(s)
N. Peart, Jason
J. Gross, Garrett
Griffith University Author(s)
Year published
2004
Metadata
Show full item recordAbstract
Controversy exists regarding the relative roles of d- and ?-opioid receptor activation as a potential cardioprotective mechanism. Furthermore, the function of opioid receptor activation in cardioprotection has not been examined in the murine heart. To this end, we employed various concentrations of selective d- and ?-opioid receptor agonists in an isolated murine heart model undergoing 20 min global ischemia followed by 45 min reperfusion. Left-ventricular developed pressure (LVDP) returned to 50.7 ᠲ.1% of baseline values in untreated hearts. Infusion of the non-selective opioid agonist, morphine (10 卩, lead to a marked ...
View more >Controversy exists regarding the relative roles of d- and ?-opioid receptor activation as a potential cardioprotective mechanism. Furthermore, the function of opioid receptor activation in cardioprotection has not been examined in the murine heart. To this end, we employed various concentrations of selective d- and ?-opioid receptor agonists in an isolated murine heart model undergoing 20 min global ischemia followed by 45 min reperfusion. Left-ventricular developed pressure (LVDP) returned to 50.7 ᠲ.1% of baseline values in untreated hearts. Infusion of the non-selective opioid agonist, morphine (10 卩, lead to a marked improvement in post-ischemic contractile recovery where LVDP returned to 65.5 ᠲ.4% of baseline function. The -opioid selective agonist BW373U86 hydrochloride elicited maximal protection at a concentration of 1 占which afforded 63.9 ᠳ.4% recovery of LVDP. This effect was blocked by the d-opioid selective antagonist, BNTX. Furthermore, administration of the ?-opioid selective agonist U50,488 (1 卩 produced a marked improvement in contractile recovery leading to a 72.5 ᠵ.3% recovery of LVDP. This degree of protection was also abolished by the d-opioid receptor antagonist, nor-BNI. No differences were noted in LDH efflux from post-ischemic hearts. These data suggest that exogenous activation of d- and ?-opioid receptors afford protection against myocardial stunning in the isolated murine heart, an effect attenuated by selective receptor antagonists.
View less >
View more >Controversy exists regarding the relative roles of d- and ?-opioid receptor activation as a potential cardioprotective mechanism. Furthermore, the function of opioid receptor activation in cardioprotection has not been examined in the murine heart. To this end, we employed various concentrations of selective d- and ?-opioid receptor agonists in an isolated murine heart model undergoing 20 min global ischemia followed by 45 min reperfusion. Left-ventricular developed pressure (LVDP) returned to 50.7 ᠲ.1% of baseline values in untreated hearts. Infusion of the non-selective opioid agonist, morphine (10 卩, lead to a marked improvement in post-ischemic contractile recovery where LVDP returned to 65.5 ᠲ.4% of baseline function. The -opioid selective agonist BW373U86 hydrochloride elicited maximal protection at a concentration of 1 占which afforded 63.9 ᠳ.4% recovery of LVDP. This effect was blocked by the d-opioid selective antagonist, BNTX. Furthermore, administration of the ?-opioid selective agonist U50,488 (1 卩 produced a marked improvement in contractile recovery leading to a 72.5 ᠵ.3% recovery of LVDP. This degree of protection was also abolished by the d-opioid receptor antagonist, nor-BNI. No differences were noted in LDH efflux from post-ischemic hearts. These data suggest that exogenous activation of d- and ?-opioid receptors afford protection against myocardial stunning in the isolated murine heart, an effect attenuated by selective receptor antagonists.
View less >
Journal Title
Basic Research in Cardiology
Volume
99
Subject
Cardiorespiratory Medicine and Haematology