Dhein S, Müller A, Klaus W
Pharmakologisches Institut, Universität zu Köln, F.R.G.
Int J Cardiol. 1990 Nov;29(2):163-72. doi: 10.1016/0167-5273(90)90218-t.
Isolated rabbit hearts, perfused according to the Langendorff technique were treated with 0.2 mumol/l ouabain or with a combination of 0.2 mumol/l ouabain and 3 nmol/l nifedipine. In a second series of experiments, a combination of 0.2 mumol/l ouabain with 0.2 mumol/l nitroglycerin was examined. Under this treatment, coronary flow and left ventricular pressure were continuously measured and, furthermore, the epicardial potential distribution was mapped with high temporal (4 kHz/channel) and spatial resolution (256 electrodes, arranged in 4 plates with 64 electrodes each, 8 x 8 matrix with 1 mm mesh size). Ouabain led to the expected positive inotropy of 10%, but also to a decrease in coronary flow of 15%. Besides these changes a nearly generalized ST-segment elevation could be observed. Moreover, the epicardial activation pattern was disturbed by changes in the location of epicardial breakthrough-points. Concomitantly, the epicardial activation vector field was deranged. Under the additional influence of nifedipine, coronary flow was reduced by only 5%, whereas the positive inotropic effect remained unchanged. The epicardial ST-elevation was diminished significantly and there was no derangement in the process of epicardial activation. Nitroglycerin led to an increase in relative coronary flow comparable to that observed under nifedipine but did not antagonize the disturbances of the process of activation by ouabain and only partially inhibited ST-elevation. Hence, it is concluded that ouabain already provokes coronary vasoconstriction in therapeutic concentrations leading to ST-elevation and prearrhythmic changes in the process of excitation. These changes could be diminished by additional treatment with nifedipine, but not with nitroglycerin.
采用Langendorff技术灌注的离体兔心，用0.2 μmol/L哇巴因或0.2 μmol/L哇巴因与3 nmol/L硝苯地平的组合进行处理。在第二系列实验中，检测了0.2 μmol/L哇巴因与0.2 μmol/L硝酸甘油的组合。在此处理下，持续测量冠状动脉血流量和左心室压力，此外，还以高时间分辨率（4 kHz/通道）和空间分辨率（256个电极，排列在4个板中，每个板64个电极，8×8矩阵，网格大小为1 mm）绘制心外膜电位分布。哇巴因导致预期的10%正性肌力作用，但也使冠状动脉血流量减少15%。除了这些变化外，还可观察到几乎普遍的ST段抬高。此外，心外膜激动模式因心外膜突破点位置的改变而受到干扰。同时，心外膜激动向量场紊乱。在硝苯地平的额外影响下，冠状动脉血流量仅减少5%，而正性肌力作用保持不变。心外膜ST段抬高明显减轻，心外膜激动过程无紊乱。硝酸甘油导致相对冠状动脉血流量增加，与硝苯地平作用下观察到的情况相当，但不能拮抗哇巴因对激动过程的干扰，仅部分抑制ST段抬高。因此，得出结论，治疗浓度的哇巴因已引起冠状动脉血管收缩，导致ST段抬高和兴奋过程中的心律失常前期变化。这些变化可用硝苯地平额外治疗减轻，但不能用硝酸甘油减轻。
