Berdeaux A, Giudicelli J F
J Pharmacol. 1985 Jan-Mar;16(1):59-74.
The effects of nicardipine, a phenyldihydropyridine calcium-channel antagonist agent, have been investigated on regional blood flow and epicardial ST-segment elevation in the nonischemic and ischemic myocardial zones after either intermittent, or permanent coronary artery occlusion in dogs. Whichever the experimental model used, nicardipine reduced heart rate and arterial blood pressure and increased regional myocardial blood flows (50 to 100% of control flow values). All these effects were dose-dependent. During intermittent coronary occlusion (a model that mimics angina pectoris), the nicardipine-induced myocardial vasodilation was homogeneous between the endocardium and the epicardium of the ischemic and nonischemic zones. During permanent coronary occlusion (a model that mimics myocardial infarction), the nicardipine-induced myocardial vasodilation mainly developed within the endocardium of the ischemic zone, leading thus to a beneficial transmural blood flow redistribution in that zone. Finally, and whichever the experimental model used, nicardipine did not reduce the ischemic injury as assessed by epicardial ST-segment elevation.
在犬类动物中,研究了苯二氢吡啶类钙通道拮抗剂尼卡地平对间歇性或永久性冠状动脉闭塞后非缺血心肌区和缺血心肌区局部血流及心外膜ST段抬高的影响。无论采用何种实验模型,尼卡地平均可降低心率和动脉血压,并增加局部心肌血流量(达到对照流量值的50%至100%)。所有这些效应均呈剂量依赖性。在间歇性冠状动脉闭塞(模拟心绞痛的模型)期间,尼卡地平诱导的心肌血管舒张在缺血区和非缺血区的心内膜和心外膜之间是均匀的。在永久性冠状动脉闭塞(模拟心肌梗死的模型)期间,尼卡地平诱导的心肌血管舒张主要发生在缺血区的心内膜内,从而导致该区域有益的透壁血流重新分布。最后,无论采用何种实验模型,通过心外膜ST段抬高评估,尼卡地平均未减轻缺血损伤。