Lasukova T V, Maslov L N, Lishmanov Iu B, Gross G J
Institute of Cardiology, Tomsk Research Center, Siberian Division, Russian Academy of Medical Sciences, ul. Kievskaya 111a, Tomsk, 634050 Russia.
Izv Akad Nauk Ser Biol. 2004 Jan-Feb(1):92-9.
The experiments on isolated rat heart demonstrated significant decrease in reperfusion-induced damage of cardiomyocytes by addition of selective delta 1 receptor agonist DPDPE (0.1 mg/l) to the perfusion solution. On the contrary, no cardioprotective effect was observed for 0.5 mg/l concentration of the peptide or after its intravenous injection. Stimulation of the cardiac delta 1 opioid receptors by intravenous injection of 0.5 mg/kg DPDPE or its addition to the perfusion solution decreased myocardial contractility both in conditions of normal oxygenation and during reperfusion. Thus, the cardioprotective and negative inotropic effect of DPDPE is mediated by activation of the cardiac delta 1 opioid receptors.
对离体大鼠心脏进行的实验表明,在灌注液中添加选择性δ1受体激动剂DPDPE(0.1毫克/升)可显著降低再灌注诱导的心肌细胞损伤。相反,对于0.5毫克/升浓度的该肽或其静脉注射后,未观察到心脏保护作用。静脉注射0.5毫克/千克DPDPE或在灌注液中添加该物质刺激心脏δ1阿片受体,在正常氧合条件下和再灌注期间均会降低心肌收缩力。因此,DPDPE的心脏保护和负性肌力作用是由心脏δ1阿片受体的激活介导的。