Bernardini N, Danesi R, Bernardini M C, Del Tacca M
Institute of Medical Pharmacology, Pisa University, Italy.
Experientia. 1988 Dec 1;44(11-12):1000-2. doi: 10.1007/BF01939901.
Doxorubicin (DXR) (0.17 x 10(-4) M) induces an acute cardiotoxicity in isolated rat heart; there is a progressive widening of the S alpha T segment, with a decrease in force derivatives and in the coronary flow. Concurrent perfusion with fructose-1,6-diphosphate (FDP) (10(-5)-10(-4) M) dose-dependently reduces the S alpha T enlargement but fails to affect the reduction in force derivatives and coronary flow. The target of cardiac protection by FDP might be the ionic mechanisms underlying the action potential configuration.
阿霉素(DXR)(0.17×10⁻⁴M)可在离体大鼠心脏中诱发急性心脏毒性;SαT段逐渐变宽,同时力导数和冠脉流量降低。同时灌注1,6 - 二磷酸果糖(FDP)(10⁻⁵ - 10⁻⁴M)可剂量依赖性地减轻SαT段增宽,但未能影响力导数和冠脉流量的降低。FDP心脏保护作用的靶点可能是动作电位形态的离子机制。