| Objective Intracerebroventricular or intrathecal injection of morphine preconditioning can reduce the myocardial ischemia / reperfusion (I / R) injury in rats, especially outside the heart of central opioid receptors may be involved in opiate substance-mediated ischemic myocardial protection, However, it was little studied that morphine preconditioning on the central means by which the anti-nociceptive signal reached peripheral, especially the heart and thus play an anti-ischemic effects . This study intended to introduce endogenous materialβ-endorphin to explore its role on cardioprotection after central morphine pretreatment in rats.Methods 250-300g, Male SD rats were established intracerebroventricular catheter placement and myocardial ischemia/reperfusion models.Ligation and open anterior descending coronary artery to achieve regional myocardial ischemia. Experiment were divided into three parts: First, to further clarify the effect of central and peripheralβ-endorphin on myocardial ischemia injury. animal were randomly assigned to sham-operated group (Sham), ischemia control group (CON), ischemic preconditioning group (IPC), the central endorphin agonist group (Icv-EP, Icv 1μg ? kg-1) and peripheral endorphin agonist group (Iv-EP, Iv 100μg ? kg-1), 6 rats in every group, in addition to the sham operation group, the rest of the group are accepted 30 min ischemia and 120 min reperfusion treatment, IPC were subjected to three cycles of 5 min of ischemia interspersed by 5 min of reperfusion; Icv-EP and Iv-EP were given intracerebroventricular and intravenousβ-endorphin agonist, 1μg ? kg-1, and 100μg ? kg-1respectively 5 min before I / R. Second, to observe theβ-endorphin in the central and peripheral levels of the different changes in the distribution in order to understand the effects of the central morphine after pretreatment on central and peripheralβ-endorphin effects. Rats were divided into sham operation group (Sham), ischemia control group (CON) and the central morphine-pretreatment group(Icv-MPC), 5 rats in each group. CON and Icv-MPC were respectively subjected to intracerebroventricular Normal saline (NS) and morphine by three consecutive 5 min drug infusions interspersed by 5 min drug free period before followed long ischemia- reperfusion ,including morphine of a total dose 1 ug ? kg-1×3. sham were like with CON except non-ischemic reperfusion. Third, to evaluate the role ofβ-endorphin blockers in the central morphine preconditioning-mediated myocardial protection. Rats were randomly divided into seven groups(n=6)and have received I / R treatment. They were subjected to CON, Icv-MPC group (like the second part), the centralβ-endorphin blockers (Icv-MPC-AEP / Icv-AEP-MPC) Group: given intracerebroventricular 100μg ? kg-1 ofβ-endorphin blockers (AEP) 5 min before and after Icv-MPC; peripheralβ-endorphin blockers (Icv-MPC + Iv-AEP) groups: recevied intravenous AEP 10 mg ? kg-1 after Icv-MPC.and its self-control group(Icv / Iv-AEP). During experiment we observed hemodynamic parameter,infart size (demonstrated by IS/AAR) ,β-endorphin RIA and positive value of the average optical density value of the reactants (MOD), the average integral optical density value ( IOD). Finnaly,all data were expressed as mean±SD. Data of different groups were analyzed using one-way analysis of variance(ANOVN) with Newman-Keuls test for multiple comparisons. Statistical differences were considered significant if the P value was <0.05.Results All groups MAP, HR, and RPP were a transient decrease during ischemia and reperfusion 30 min and 120 min, but to compare between the two groups was not statistically significant (P <0.05).The reduction in IS/AAR with central and peripheral administration ofβ-EP (17.91 %±2.05 % and 18.55 %±3.29 %) was similar to that produced by IPC (12.47 %±2.39 %) and they were reduced significantly versus 53.49 %±13.07 % for the control group (P < 0.01). Icv-MPC-AEP abolished protective effect of Icv-MPC(P <0.01), but there was also difference compared with control group(P <0.05);Icv-AEP-MPC and Icv-MPC + Iv-AEP group (IS / AAR were 20.62 %±4.15 %, 21.65 %±4.39 %) had no effect on Icv-MPC-mediated myocardial protection (P > 0.05); self-control group of the IS / AAR were 45.66 %±11.60 % and 55.22 %±11.56 %. Moreover, In Icv-MPC ,where level ofβ-EP in the plasma and pituitary gland were increased in chorus ,IOD and MOD were also decreased in ARC (P < 0.05) and increased significantly in PAG and MC versus CON(P < 0.05;P < 0.01);while the Sham group was changed inversely.Conclusions Myocardial post-ischemic injury was attenuated by central and peripheral administration ofβ-EP in rats. Our results suggest that endorphinergic systems activation in central nervous system and promoting theβ-EP released from ARC may partly as a neurotransmitter involved in central morphine preconditioning -induced cardioprotection.
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