右旋美托咪定后处理对大鼠心肌缺血再灌注损伤的保护作用

目的：评价右旋美托咪定（DEX）后处理对大鼠心肌缺血再灌注时Na⁺-K⁺-ATP酶和Ca²⁺-ATP酶活性的影响。方法：36个成年雄性Wistar大鼠心脏置于改良的Langendoff装置上，均为平衡灌注末HR>180次/min、左室收缩压>75mm Hg、室性早搏<2个/min的心脏模型，采用随机数字表法分为3组：对照组（A组）、缺血再灌注组（B组）、DEX处理组（C组），每组12个。A组持续灌注KH液180 min，B组和C组在KH平衡灌注20 min时常温停灌40 min后恢复灌注，于再灌注即刻分别灌注KH液、含100 nmol·L^-1 DEX的KH液20 min，然后继续再灌注KH液100 min。监测心率（HR）、冠状动脉流出量（CF），左心室发展压（LVDP）、左心室内压最大上升和下降速率（±dP/dt_max），采用酶联免疫法测定心肌Na⁺-K⁺-ATP酶、Ca²⁺-ATP酶，以梗死心肌质量占心室质量的百分比表示心肌梗死率。结果：再灌注后A组心功能优于B组、C组（P<0.05），C组优于B组（P<0.05）。与A组比较，B组和C组心肌梗死率较大，心肌组织Na⁺-K⁺-ATP酶、Ca²⁺-ATP酶的活性降低（P<0.05）；与B组比较，C组心肌梗死率低，心肌组织Na⁺-K⁺-ATP酶、Ca²⁺-ATP酶的活性较高（P<0.05）。结论：DEX后处理可提高Na⁺-K⁺-ATP酶和Ca²⁺-ATP酶的活性，减轻大鼠心肌缺血再灌注损伤。

Effects of dexmedetomidine postconditioning on activities of ATPase during myocardial ischemia-reperfusion in rats

OBJECTIVE To investigate effects of dexmedetomidine postconditioning on activities of Na⁺-K⁺-ATPase and Ca²⁺-ATPase during myocardial ischemia-reperfusion (I/R) in rats and possible mechanism.METHODS Hearts of 36 healthy male Wistar rats were placed onto modified Langendoff system,all with HR>180/min,left ventricular systolic pressure >75mm Hg and premature ventricular beat<2/min.Then hearts were randomly divided into 3 groups:control group (A),ischemia reperfusion group (B) and DEX treated group (C).Each group included 12 hearts.Hearts in group A were continuously perfused KH solution for 180min,while hearts in group B and C were perfused with KH solution for 20min,then discontinued for 40min under normal temperature,and then continued perfusion with KH solution,KH solution with 100 nmol·L^-1 DEX,and then KH solution for 100 min.Heart rate (HR),coronary flow (CF),left ventricular development pressure (LVDP),maximal descending and declining rate of left ventricular pressure (dP/dt_max) were monitored,Na⁺-K⁺-ATPase and Ca²⁺-ATPase were determined by enzyme linked immunosorbent assay,and percentage of infarcted myocardial mass to ventricular mass was used to indicate myocardial infarction rate.RESULTS Infarct size was significantly larger and activities of Na⁺-K⁺-ATPase and Ca²⁺-ATPase were significantly lower in group B than in group A (P<0.05).Infarct size was significantly smaller and activities of Na⁺-K⁺-ATPase and Ca²⁺-ATPase were significantly higher in group C than in group B (P<0.05).CONCLUSION Dexmedetomidine postconditioning can reduce myocardial I/R injury through increasing activities of Na⁺-K⁺-ATPase and Ca²⁺-ATPase.