关键词: 缺灌损伤, 再灌损伤, 乳酸脱氢酶, 苯丙氨酸, 硫辛酸

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