Ichihara K, Morimoto T, Tsujitani M, Abiko Y
Department of Pharmacology, Asahikawa Medical College, Japan.
J Pharm Pharmacol. 1993 Feb;45(2):131-6. doi: 10.1111/j.2042-7158.1993.tb03697.x.
The effects of LP-805, a newly developed vasodilator, on changes in the myocardial energy and carbohydrate metabolism induced by ischaemia were studied in open-chest anaesthetized dogs. Ischaemia was induced by ligating the left anterior descending coronary artery for 3 min. The myocardial energy stores were depleted, and the levels of glycolytic intermediates were altered 3 min after the onset of ischaemia. Energy change potential was decreased, and ([G6P] + [F6P])/[FDP] and [lactate]/[pyruvate] ratios were increased by ischaemia. These findings indicated that the myocardial metabolism was converted from an aerobic to an anaerobic type by ischaemia. LP-805 (10, 30, or 100 micrograms kg-1) was injected intravenously 5 min before the onset of ischaemia. LP-805 prevented the myocardial energy depletion and alterations of myocardial carbohydrate metabolism due to ischaemia, indicating that it appeared to convert the anaerobic metabolism back to aerobic metabolism in the ischaemic myocardium. In conclusion, LP-805 may reduce the ischaemic influence on the myocardium.
在开胸麻醉犬身上研究了新开发的血管扩张剂LP - 805对缺血诱导的心肌能量和碳水化合物代谢变化的影响。通过结扎左冠状动脉前降支3分钟诱导缺血。缺血开始3分钟后，心肌能量储备耗尽，糖酵解中间产物水平发生改变。缺血使能量变化潜能降低，([G6P] + [F6P])/[FDP]和[乳酸]/[丙酮酸]比值升高。这些发现表明缺血使心肌代谢从有氧型转变为无氧型。在缺血开始前5分钟静脉注射LP - 805(10、30或100微克/千克)。LP - 805可防止缺血导致的心肌能量耗竭和心肌碳水化合物代谢改变，表明它似乎能使缺血心肌的无氧代谢恢复为有氧代谢。总之，LP - 805可能减轻缺血对心肌的影响。
