Preusse C J, Gebhard M M, Schnabel A, Ulbricht L J, Bretschneider H J
J Cardiovasc Surg (Torino). 1984 Mar-Apr;25(2):158-64.
The influence of pre-ischemic treatment with propranolol (0.8 mg/kg bw) or with verapamil (0.1 mg/kg bw) on myocardial O2 consumption and on coronary resistance after cardioplegic arrest (300 minutes at 22 degrees - 24 degrees C) was investigated, using a Langendorff technique in open chest experiments (canine hearts). For myocardial protection histidine buffered Bretschneider solution was used, while for standardization all hearts were postischemically reperfused with a modified Tyrode solution at 35 degrees C. Both drugs were given intravenously in two fractions, 60 and 30 minutes before the onset of cardioplegic perfusion; a third group was not pretreated. Although the verapamil group had the lowest O2 consumption post-ischemically, the most impressive results were found in coronary resistance. Propranolol significantly diminished coronary resistance (p less than 0.05), while verapamil distinctly enhanced it compared to the non treated group. The "membrane labilizing" effect of verapamil combined with calcium-free cardioplegic solution was confirmed by a massive postischemic myocardial sodium uptake.
在开胸实验（犬心）中，采用Langendorff技术，研究了用普萘洛尔（0.8毫克/千克体重）或维拉帕米（0.1毫克/千克体重）进行缺血预处理对心脏停搏（22摄氏度至24摄氏度下300分钟）后心肌氧耗和冠状动脉阻力的影响。心肌保护采用组氨酸缓冲的布雷施奈德溶液，为进行标准化，所有心脏在缺血后均用35摄氏度的改良台氏液再灌注。两种药物均分两次静脉给药，在心脏停搏灌注开始前60分钟和30分钟给药；第三组未进行预处理。尽管维拉帕米组缺血后氧耗最低，但冠状动脉阻力方面的结果最为显著。普萘洛尔显著降低了冠状动脉阻力（p<0.05），而与未治疗组相比，维拉帕米明显增加了冠状动脉阻力。维拉帕米与无钙心脏停搏液联合使用的“膜稳定”作用通过缺血后心肌大量摄取钠得以证实。
