Objective Recently it has been demonstrated that intracerebroventricular morphine preconditioning(MPC) could confer protection against injury induced by ischemia in the intact rat heart. To investigate the involvement of adenosine in spinal cord and myocardial in cardioprotective effect of intracerebroventricular morphine preconditioning on rat's myocardial ischemia reperfusion injury, and the relationship with the inflammatory reaction of ischemia-reperfusion injury.Methods 54 Male Sprague-Dawley rats with intrathecal and intracerebroventricular catheter placement were randomly assigned to 1 of 5 groups (n=12): Sham group; control group; MPC group; MPC+THE group; and THE group. Indicators to be observed are composed of MAP, HR and RPP (MAPĂ—HR); Infarct size (IS), as a percentage of the area at risk, was determined by 2, 3, 5-triphenyltetrazolium staining, the volume of area at risk (AAR) , and the area of myocardial infarction, which is demonstrated by IS/AAR; And also the intercellular adhesion molecules (ICAM-1) expression in myocardium was determined by immunohistochemical method. HPLC determined the level of adenosine in myocardial.Results Compared with control group, the volume of IS and IS/AAR both declined in MPC group and MPC+THE group ( P < 0.01) ,But the volume of IS and IS/AAR of MPC+THE group is higher than MPC group(P < 0.01). There is no significant difference between THE group and control group (P>0.05). ICAM-1 express in myocardium of control group were higher than Sham group, MPC group and MPC+THE group.(P < 0.01). Compared with MPC group, ICAM-1 expressed in myocardium of MPC+THE group is much more(P < 0.01).The level of adenosine in control group is higher than Sham group, but lower than MPC group (P < 0.01). The level of adenosine in MPC+THE group is apparently lower than MPC group (P < 0.01), but higher than control group(P < 0.05).Conclusion Intracerebroventricular morphine up-regulated activation of adenosine receptor in spinal cord and the level of adenosine in myocardial, the latter suppressed the inflammatory reaction of ischemia-reperfusion injury, and partly mediated the cardioprotective effect of intracerebroventricular morphine preconditioning by this way. |