N-Methyl-1-deoxynojirimycin (MOR-14), an α-glucosidase inhibitor, markedly improves postischemic left ventricular dysfunction

摘要: We examined whether pharmacological inhibition of glycogenolysis by N-methyl-1-deoxynojirimycin (MOR-14), a new compound which reduces the glycogenolytic rate inhibiting α-1,6-glucosidase activity glycogen-debranching enzyme, can protect heart against postischemic left ventricular dysfunction. The hearts male Sprague-Dawley rats were excised, and perfused on Langendorff apparatus with Krebs-Henseleit solution gas mixture 95% O2 5% CO2. paced at 320 beats/min except during ischemia. Left developed pressure (LVDP, mmHg), ±dP/dt (mmHg/s), coronary flow (ml/min) continuously monitored. All for total 120 min including 30-min preischemic period followed episode global ischemia 60 reperfusion, or without 0.5 2 mM MOR-14 first 30 reperfusion. In another series experiments, myocardial content glycogen lactate was measured in groups treated MOR-14. Preischemic but not treatment significantly improved LVDP altering reperfusion dose-dependent manner. preserved attenuated accumulation is protective dysfunction through isolated rat heart.