Kahles H, Junggeburth J, Lick T, Schäfer W, Kochsiek K
Medical Clinic, University of Würzburg, Fed. Rep. of Germany.
Arzneimittelforschung. 1987 Oct;37(10):1137-40.
The effect of N(6)-phenyl-N(6)-allyladenosine (PAA, BM 11.189) on myocardial ischemic stress was evaluated in six open-chest mongrel dogs during repeated coronary occlusions of 3 min. Whereas there was not significant change in hemodynamic parameters before and during coronary occlusions after treatment, PAA reduced significantly epicardial ST-segment elevations (-34%) during ischemia and myocardial release of lactate (-43%), phosphate (-44%), and potassium (-48%) in the early reperfusion period. PAA lowered significantly arterial non esterified fatty acids and converted oxidative myocardial metabolism from lipid to predominantly carbohydrate utilization, reflected by a shift of cardiac respiratory quotient from 0.81 to 1.01. The beneficial effects of PAA on myocardial ischemic injury could be explained by an improved economy of oxidative myocardial energy supply in the jeopardized border zone of the ischemic myocardium.
在六只开胸杂种犬身上,于重复3分钟冠状动脉闭塞期间,评估了N(6)-苯基-N(6)-烯丙基腺苷(PAA,BM 11.189)对心肌缺血应激的影响。治疗后冠状动脉闭塞前和闭塞期间血流动力学参数无显著变化,但PAA在缺血期间显著降低了心外膜ST段抬高(-34%),并在再灌注早期显著降低了心肌乳酸(-43%)、磷酸盐(-44%)和钾(-48%)的释放。PAA显著降低了动脉非酯化脂肪酸水平,并使心肌氧化代谢从脂质利用转变为主要利用碳水化合物,心脏呼吸商从0.81变为1.01即反映了这一点。PAA对心肌缺血损伤的有益作用可通过改善缺血心肌濒危边缘区心肌氧化能量供应的经济性来解释。