Myocardial protective effect of acetylcholine against ischemia/reperfusion injury and its underlying mechanism / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To determine whether the caidioprotection of acetylcholine (ACh) against ischeniia/reperftision (I/R) injury is re-kited to mitochondrial permeability transition pore (MEW) and mitochondrial AW-sensitive potassium channel (mitoK(ATP)).</p><p><b>METHODS</b>Male Sprague-Dawley rats were used for Langendorif isolated bean perkision. The hearts were subjected to global ischemia for 30 mm followed by 120 rein of reperfusion and the left ventricular hemodynaniic parameters were measured. Formazan, a product of 2,3, 5-triphenyl-tetrazolium chloride (TTC), which is proportional to myocardial viability, was measured at 490 nm, and the level of lactate dehydrogenase (LDH) in the coronary effluent was measured to evaluate the cardiac injury.</p><p><b>RESULTS</b>The pretreatment with ACh (0.1 mol/L, 5 mm) before I/R markedly increased myocardial formazan content, reduced LDH release, improved the recovery of the left veritficular developed pressure, +/- dP/dtmax, and rate pressure product (left ventricular developed pressure multiplied by hean rate) and attenuated the decrease of coronary flow during reperfusion. The opener of MPTP, atiractyloside (20 mmoL/L) or the inhibitor of mitoK(ATP), 5-hydroxydecanoate (100 micromol/L) abolisbed the beneficial effect of ACh.</p><p><b>CONCLUSION</b>In the isolated rat bean, ACh protects myocardium against ischemia/reperfusion injury via inhibiting the opening of MPTP and increasing the opening of mitoKATP in heart.</p>

Delta-opioid receptor mediates the cardioprotective effect of ischemic postconditioning / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effect of 8-opioid receptors in the cardioprotection elicited by ischemic postconditioning and the underlying mechanism.</p><p><b>METHODS</b>The isolated perfused hearts of male Sprague-Dawley rats were subjected to 30 min of global ischemia followed by 120 min of reperfusion. Formazan content of myocardium was measured spectrophotometrically, and the activity of lactate dehydrogenase (LDH) in the coronary effluent was measured. In isolated ventricular myocytes hypoxic postconditioning was achieved by 3 cycles of 5 min reoxygenation/5 min hypoxia starting at the beginning of reoxygenation, and cell viability was measured.</p><p><b>RESULTS</b>In the Langendorff perfused rat heart model, ischemic postconditioning (6 cycles of 10 s reperfusion/10 s global ischemia starting at the beginning of reperfusion) increased formazan content, reduced LDH release, improved the recovery of the left ventricular developed pressure, maximal rise/fall rate of left ventricular pressure and rate pressure product (left ventricular developed pressure multiplied by heart rate), attenuated the decrease of coronary flow during reperfusion and increased the isolated cell viability. Pretreatment with naltrindole, an antagonist of delta-opioid receptors and calcium-activated potassium channel (KCa) blocker paxilline attenuated the effect of ischemic/hypoxic postconditioning.</p><p><b>CONCLUSION</b>The findings indicate that ischemic postconditioning protects myocardium against ischemia/reperfusion injury via activating delta-opioid receptors and opening KCa.</p>