[Effect of dexmedetomidine postconditioning on myocardial ischemia-reperfusion injury and inflammatory response in diabetic rats].

OBJECTIVE: To investigate the effect of dexmedetomidine postconditioning in alleviating myocardial ischemia-reperfusion (IR) injury and inflammation in diabetic mellitus rats. METHODS: Thirty normal male Sprauge Dawley (SD) rats were randomly allocated into 3 groups (n=10), namely the sham-operated group, IR group, and dexmedetomidine postconditioning (DP) group. Similarly, another thirty diabetic SD rats were also randomly allocated into diabetic sham (DM-S) group, diabetic IR (DM-IR) group and diabetic dexmedetomidine postconditioning (DM-DP) group. The mean arterial pressure (MAP), heart rate (HR) and the rate pressure product (RPP) were recorded at baseline, after 30 min of ischemia, and at 30 and 120 min during reperfusion. Myocardial infarct size was analyzed by TTC double staining method, and plasma levels of CTnI, TNF-a, IL-6, IL-10 and IL-1β were measured at 120 min of reperfusion. RESULTS: Compared with those in the sham-operated group, normal and diabetic rats in IR and DP groups showed significantly lowered MAP, HR, and RPP and increased levels of plasma CTnI, TNF-a, IL-6, IL-10 and IL-1β levels after 30 min of ischemia and at 30 min and 120 min of reperfusion (P<0.05). Compared with those in the IR group, the normal rats in DP group showed decreased MAP, HR, and RPP at 30 min of ischemia and at 30 min of reperfusion, which increased at 120 min of reperfusion (P<0.05); the infarct size and plasma CTnI, TNF-a, IL-6 and IL-1β levels were decreased while IL-10 was increased in DP group (P<0.05). Compared with those in DP group, the rats in DM-DP group showed similar MAP, HR and RPP (P>0.05) but significantly increased infarct size and plasma CTnI, TNF-a, IL-6 and IL-1β levels (P<0.05). CONCLUSION: Dexmedetomidine postconditioning may produce a cardioprotective effect against myocardial IR injury in normal rats by alleviating inflammation, but can not reduce the release of inflammatory mediators in diabetic rats to improve myocardial infarction.