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实验以离休灌流的SD大鼠心脏为模型，用k特异性桔抗剂MR2266研究k阿片受体的阻断与缺血预处理（IP）的关系，用放射免疫分析法研究IP及长时间缺血对心肌强啡肽A1-13（DynA1－13）浓度的影响，探索K阿片物质在IP过程中的作用和地位。结果显示：（1）IP可减轻缺血／复灌性心律失常严重程度（P＜0．05），缩小心肌梗死范围（P＜0．01），对冠脉流量和心率无明显影响;（2）MR2266可减轻缺血／复灌性心律失常严重程度（P＜0．05），缩小心肌梗死范围（P＜0．01），促进复灌过程中冠脉流量的恢复，对心率无明显影响；（3）空白灌流对照组心房肌DynA1－13浓度（pg/mg心肌湿重）为1.14±0．44，有IP的长时间缺血组和无IP的长时间缺血组心房肌DynA1－13浓度分别为05±0．23和0．41±0.14；对照组心室肌浓度为0．76±0．25，有IP的长时间缺血组和无IP的长时间缺血组心室肌DynA1－13浓度分别为0．49±0.24和0.28±0．09。可见缺血使DynA1-13浓度降低（P＜0.05），缺血前未经过IP处理的心脏这种降低较之经过IP处理的心脏更明显（P＜0．05）。结果提示：（1）k阿片受体拮抗剂MR2266能“模拟”IP的抗心律失常作用和缩小心肌梗死范围；（2）缺血可能引起k阿片物质释放，经过IP处理的心肌在随后较长时间缺血时释放的内源
In the present study, the heart of SD rats subjected to reperfusion was used as a model. The relationship between blockade of k opioid receptor and ischemic preconditioning (IP) was investigated by k22-specific antagonist MR2266. Radioimmunoassay was used to study the relationship between IP and prolonged absence Effects of Blood on the Concentration of Myocardial Dynorphin A1-13 (DynA1-13) and the Role and Position of K Opioid in IP. The results showed that: (1) IP attenuated the severity of ischemia / reperfusion arrhythmia (P <0.05), reduced the range of myocardial infarction (P <0.01) and had no effect on coronary flow and heart rate; ( 2) MR2266 can reduce the severity of ischemia / reperfusion arrhythmia (P <0.05), reduce the range of myocardial infarction (P <0.01), and promote the recovery of coronary flow during reperfusion, (3) DynA1-13 concentration (pg / mg wet weight) in atrial perfusion control group was 1.14 ± 0.44 in blank perfusion control group, and the long-term ischemic group with IP and the long-term ischemic group without IP had DynA1 -13 were 05 ± 0.23 and 0.41 ± 0.14, respectively. The control group had a ventricular concentration of 0.76 ± 0.25. The long-term ischemia group with IP and the long-term ischemic group without IP had ventricular DynA1-13 concentrations were 0.49 ± 0.24 and 0.28 ± 0.09, respectively. Visible ischemia decreased the concentration of DynA1-13 (P <0.05). The decrease in IP-treated hearts before ischemia was more pronounced than in IP-treated hearts (P <0.05). The results suggest that: (1) k opioid receptor antagonist MR2266 can “mimic” the anti-arrhythmic effects of IP and narrow the range of myocardial infarction; (2) ischemia may cause the release of k opioid, IP-treated myocardium in the subsequent longer Endogenous release of time when ischemia