Izv Akad Nauk Ser Biol. 2005 Jan-Feb(1):55-62.
Activation of cardiac delta-opioid receptors (ORs) by their selective agonist DPDPE (154 nM) increased the resistance of perfused rat heart to ischemia/reperfusion. Decreased release of creatine phosphokinase to the perfusate and decreased occurrence of arrhythmia were observed during reoxygenation. At the same time, opioidergic decrease in left ventricular developed pressure took place both during the preischemic period and after restoring the coronary circulation. All these effects could be prevented by blocking delta-ORs by naltrindole or inhibition of Ca2+ -ATPase of sarcoplasmic reticulum by cyclopiazonic acid. Delta-OR agonist DPDPE had no effect on cAMP levels in myocardial tissue during the whole experiment. The obtained data suggest that the antiarrhythmic and cytoprotective effects observed after delta-OR stimulation can be realized through the changes in Ca2+ transport at the level of the sarcoplasmic reticulum.
其选择性激动剂DPDPE(154 nM)激活心脏δ-阿片受体(ORs)可增加灌注大鼠心脏对缺血/再灌注的耐受性。在复氧期间,观察到灌注液中肌酸磷酸激酶释放减少以及心律失常发生率降低。同时,在缺血前期和恢复冠状动脉循环后,左心室舒张末压均出现阿片能降低。用纳曲吲哚阻断δ-ORs或用环匹阿尼酸抑制肌浆网的Ca2+ -ATP酶可防止所有这些效应。在整个实验过程中,δ-OR激动剂DPDPE对心肌组织中的cAMP水平无影响。所得数据表明,δ-OR刺激后观察到的抗心律失常和细胞保护作用可通过肌浆网水平上Ca2+转运的变化来实现。