Abstract: Using Langendorff method, isolated mouse heart was perfused with Krebs-Hensleit (K-H) buffer solution. After 10 min of equilibrium, the heart underwent 10 min of global ischemia followed by 10 min of reperfusion. At the same time, the coronary effluents were collected in accordance with certain time intervals toanalyze lactate dehydrogenase (LDH) activity (U.L^-1) as an index of cellular damage induced by ischemic reperfusion. During 10 min ischemic(noperfusion) period, LDH release was decreased significantly in phenylalanine (Phe, 10, 1 and 0.1 micro mol.L) and lipoic acid (LA, 1 micor mol.L) treated groups compared with control group. Then in the early reperfusion period administration of Phe and LA markedly reduced the first peak and also diminished the second peak. The incidence of ventricular tachycardia (VT) was eliminated and thenumber of permature ventricular contraction (PVC) was decreased aswell as the normal sinus rhythm time (NSRT) was prolonged by the treatment of Phe. Similar results obtained from LA treatment group indicating that both substances might affected hearts through similar mechanism against ischemia reperfusion injury, e.g., the capability of oxygen free radical scavenger effect. Further development of this capability would be enable Phe and LA becoming prospective drugs in the clinic practice.

Key words: ischemia (noperfusion) injury, reperfusion injury, lactate dehydrogenase, phenylalanine, lipoic acid

摘要： 在Langendorff法灌流小鼠心脏上，以乳酸脱氢酶(LDH)释放的活性浓度(UL^-1)作为心肌细胞损伤的指标，研究苯丙氨酸(Phe)对缺灌再灌心脏的保护作用。3种不同浓度的Phe(10μmol·L^-1, 1μmol·L^-1,和0.1μmol·L^-1) 均使缺灌期LDH释放明显下降，再灌早期LDH释放第Ⅰ峰也显著下降, 并消除LDH释放第Ⅱ峰。此外，Phe还具有消除再灌期室速，抑制室性早搏和延长正常窦性节律时间的作用。Phe的保护作用与硫辛酸(LA)之作用相似。推测与淬灭缺灌再灌期间产生的氧自由基有关。

关键词: 缺灌损伤, 再灌损伤, 乳酸脱氢酶, 苯丙氨酸, 硫辛酸