右美托咪定后处理对糖尿病大鼠心肌缺血再灌注损伤及炎症反应的影响

Objective To investigate the effect of dexmedetomidine postconditioning in alleviating myocardial ischemiareperfusion (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 at30and120minduringreperfusion.MyocardialinfarctsizewasanalyzedbyTTCdoublestainingmethod,andplasmalevels of CTnI, TNF-a, IL-6, IL-10 and IL-1 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-1 levels after 30 min of ischemia and at 30 min and 120 min of reperfusion (P<0.05). Compared with those in the IRgroup, the normal rats in DPgroup showed decreasedMAP, 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-1 levels were decreased while IL-10 was increased in DP group (P0.05) but significantly increased infarct size and plasma CTnI, TNF-a, IL-6 and IL-1 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 diabeticratstoimprovemyocardialinfarction.