Parratt J R, Udvary E
Br J Pharmacol. 1983 Sep;80(1):95-105. doi: 10.1111/j.1476-5381.1983.tb11054.x.
A model is described (anaesthetized, open-chest cats subjected to acute coronary artery occlusion) which allows the effects of drug interventions to be determined on one major electrocardiographic index of myocardial ischaemia. Epicardial ST-segment changes were continuously recorded from five individual sites on the surface of the left ventricle. Coronary artery occlusion (left anterior descending branch) resulted in marked and consistent elevations of the ST-segment in all sites in nearly all experiments. These changes started within 1 min of the onset of ischaemia and reached a peak at between 30 and 60 min; thereafter there was a gradual reduction over the next 4 h. The one significant haemodynamic effect of coronary artery occlusion was an increase in left ventricular (LV) end-diastolic pressure (LVEDP). Ventricular ectopic activity was not pronounced in this model (about 50 ectopic beats over the initial 30 min post-occlusion period). Exaprolol (1.0 mg kg-1, intravenously) a potent beta-adrenoceptor blocking agent with 'membrane stabilising activity', when given 1 h after the onset of ischaemia, reduced heart rate and LV dP/dtmax and increased LVEDP. These effects were prolonged (i.e. little recovery in heart rate 3 h after administration). Exaprolol decreased total ST-segment elevation immediately after administration; this was significantly different from the effect of intravenous saline and lasted for at least 3 h. The effects appeared to be greater at sites of less pronounced ischaemia. Intramyocardial temperature records were taken to indicate a reduction in blood flow to the ischaemic region; however the alleviation of epicardial ST-segment elevation suggests an improved myocardial oxygen demand:supply ratio. Reperfusion was unsuccessfully attempted after a 4 h occlusion period; reperfusion after a shorter period (30 min) resulted in ventricular ectopic activity but no fibrillation.
本文描述了一种模型（对麻醉开胸猫进行急性冠状动脉闭塞），该模型可用于确定药物干预对心肌缺血的一项主要心电图指标的影响。从左心室表面的五个独立部位连续记录心外膜ST段变化。在几乎所有实验中，冠状动脉闭塞（左前降支）均导致所有部位的ST段显著且一致地抬高。这些变化在缺血开始后1分钟内开始，在30至60分钟时达到峰值；此后在接下来的4小时内逐渐降低。冠状动脉闭塞的一个显著血流动力学效应是左心室舒张末期压力（LVEDP）升高。该模型中的室性异位活动不明显（闭塞后最初30分钟内约有50次异位搏动）。艾司洛尔（1.0毫克/千克，静脉注射）是一种具有“膜稳定活性”的强效β-肾上腺素受体阻滞剂，在缺血开始1小时后给予，可降低心率和LV dP/dtmax，并增加LVEDP。这些作用持续时间较长（即给药后3小时心率几乎没有恢复）。艾司洛尔给药后立即降低了总的ST段抬高；这与静脉注射生理盐水的效果有显著差异，且持续至少3小时。在缺血不太明显的部位，这些作用似乎更大。记录心肌内温度以表明缺血区域血流量减少；然而，心外膜ST段抬高的减轻表明心肌氧供需比得到改善。在闭塞4小时后尝试再灌注未成功；较短时间（30分钟）后再灌注导致室性异位活动，但未发生颤动。
