Department of Cardiology, the First Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Am J Med Sci. 2013 Feb;345(2):129-35. doi: 10.1097/MAJ.0b013e31824ceba7.
Kappa-opioid receptors (κ-OR) and mechanoelectric feedback seem to have common pathways that influence electrophysiological changes resulting from acute myocardial infarction (MI). This study aims to determine the effects of the κ-OR on stretch-induced electrophysiological changes after acute MI.
Male Sprague-Dawley rats were randomly divided into 4 groups: sham operated, MI, U-50488H (a selective κ-OR agonist) -treated MI (MI+U-50488H) and nor-BNI (a selective κ-OR antagonist) -treated MI (MI+nor-BNI). After Langendorff perfusion to maintain stabilization, a transient stretch (5 seconds) was delivered early in diastole. Electrophysiological changes were recorded for 1 minute before and after stretch. Similarly, the 20%, 50% and 90% monophasic action potential duration (MAPD20, MAPD50 and MAPD90, respectively) and stretch-induced arrhythmias were recorded.
MAPD90 significantly increased in all 4 groups. MAPD90 in the MI and MI+nor-BNI groups increased significantly before stretch (P < 0.05) and after stretch (P < 0.01) but was reversed in the MI+U-50488H group (P > 0.05). MAPD90 in the MI group was increased compared with that of the MI+U-50488H group but decreased compared with that of the MI+ nor-BNI group after stretch (P < 0.01). The arrhythmia score in the MI and MI+nor-BNI groups was higher than that of the sham-operated group (P < 0.01), and the arrhythmia score in the MI+nor-BNI group was higher than that in MI group after stretch (P < 0.01). The arrhythmia score of the MI+U-50488H group was lower than that of MI group after stretch (P < 0.01).
The κ-OR could influence the stretch-induced electrophysiological changes and play an antiarrhythmic role in stretch-induced arrhythmias after acute MI.
κ-阿片受体（κ-OR）和机械电反馈似乎有共同的途径，影响急性心肌梗死（MI）后电生理变化。本研究旨在确定κ-OR 对急性 MI 后牵张诱导电生理变化的影响。
雄性 Sprague-Dawley 大鼠随机分为 4 组：假手术组、MI 组、U-50488H（选择性 κ-OR 激动剂）治疗的 MI 组（MI+U-50488H）和 nor-BNI（选择性 κ-OR 拮抗剂）治疗的 MI 组（MI+nor-BNI）。Langendorff 灌流稳定后，舒张早期给予短暂牵张（5 秒）。牵张前后记录 1 分钟的电生理变化。同样，记录 20%、50%和 90%单相动作电位时程（MAPD20、MAPD50 和 MAPD90）和牵张诱导的心律失常。
四组 MAPD90 均显著增加。MI 和 MI+nor-BNI 组牵张前（P<0.05）和牵张后（P<0.01）MAPD90 均显著增加，但 MI+U-50488H 组逆转（P>0.05）。MI 组牵张后 MAPD90 高于 MI+U-50488H 组（P<0.01），低于 MI+nor-BNI 组（P<0.01）。MI 和 MI+nor-BNI 组心律失常评分高于假手术组（P<0.01），MI+nor-BNI 组牵张后高于 MI 组（P<0.01）。MI+U-50488H 组牵张后心律失常评分低于 MI 组（P<0.01）。
κ-OR 可影响牵张诱导的电生理变化，在急性 MI 后牵张诱导的心律失常中发挥抗心律失常作用。
