| Objective:To investigate the effect of ?2 receptor on dexmedetomidine in alleviating myocardial ischemia-reperfusion injury in rats.Methods:Fifty healthy male SD rats were randomly divided into 5 groups(n = 10): Ischemia group(IR group),dexmedetomidine pretreatment group(DP group),dexmedetomidine + yohimbine pretreatment group(DY group),yohimbine pretreatment group(YP group),Sham operation group(CS group).By ligation of left coronary artery occlusion caused by myocardial ischemia,myocardial ischemia after 30 min,modeling success,The drug pretreatment group(DP / DY / YP)was injected intraperitoneally with 5ml drug solution(Drug concentration : containing dexmedetomidine 5ug / kg of normal saline;containing yohimbine 500 ug / kg of normal saline).IR group was injected intraperitoneally with 5ml saline as control,While CS group only threading ligation 150 min,intraperitoneal injection of 5ml normal saline,120 min after reperfusion induced.The changes of heart rate and mean arterial pressure were observed and recorded in each experimental group.To observe the changes of myocardial histopathology in each experimental group and calculate the area of myocardial infarction in the heart of rats at the end of reperfusion,The contents of malondialdehyde(MDA)and superoxide dismutase(SOD)in myocardium homogenate were measured.And the levels of IL-6 and TNF-? in serum and myocardium were measured by enzyme-linked immunosorbent assay.Results:1.DP group and DY group,after 30 minutes of administration,the heart rate decreased significantly,P <0.05,with the continuation of the experiment,rat heart rate showed a downward trend,but the heart rate of the DP group increased after 120 minutes of reperfusion;Compared with IR group,DP group at each time heart rate decreased,P <0.05.Compared with the sham group CS group at all times,IR group,DY group and YP group 30 minutes after ischemia,the average arterial pressure was significantly lower,P <0.05;DP group in T1-T3 average arterial pressure gradually decreased,compared with IR group,P <0.05.2.In this study,IR induced myocardial infarction(p <0.05,IR vs.CS)compared with CS.However,compared with the IR group,DEX pretreatment significantly reduced the infarct size(p <0.05,DP vs.IR).In addition,yohimbine,selective?2 adrenergic receptor antagonist,greatly attenuated by DEX treatment achieved a reduction in infarct size(p <0.05,DY vs.DP),whereas simple yohimbine did not show any detectable The effect of infarct size(p> 0.05,YOH on IR).Thus,we conclude that DEX pretreatment significantly reduces the size of myocardial infarction induced by IR.(P <0.05,DY vs.DP)was statistically significant(P <0.05).Conclusion: The expression of?2 adrenergic receptor antagonist,greatly attenuated by DEX treatment.3.The content of MDA and SOD in myocardium homogenate were significantly higher than those in CS group,the content of MDA in the myocardium of IR group increased and the activity of SOD decreased(P <0.05).Compared with IR group,the content of MDA in the myocardial homogenate of DP group increased and the activity of SOD decreased(P <0.05).The protective effect of dextromethorphan-tropicin-tropicin can reverse these protective effects of dexmedetomidine(P <0.05),The experimental results were statistically significant.4.Compared with CS group,the levels of IL-6 and TNF-? in serum and myocardium of IR group were significantly increased(p <0.05).The levels of IL-6 and TNF-? in DEX pretreatment group were significantly decreased(p <0.05 DEX to IR).And yohimbine partially reversed this effect(p <0.05,DEX / YOH vs.DEX)Conclusion:1.Pretreatment with dexmedetomidine in the heart of rats can reduce hemodynamic changes,stabilize hemodynamics,and reduce the degree of myocardial infarction,with a certain degree of myocardial protection;2.DEX pretreatment by reducing inflammation to reduce part of myocardial ischemia-reperfusion injury.3.The effect of dexmedetomidine on the myocardial ischemia-reperfusion injury was induced by dexepamidine. |
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