Fiedler V B
Basic Res Cardiol. 1984 Jan-Feb;79(1):17-26. doi: 10.1007/BF01935803.
The thrombolytic and hemodynamic properties of intracoronary streptokinase (SK) application were studied in an in-vivo canine model with left circumflex coronary artery thrombosis, initiated by electrical stimulation (150 microA, DC for 6 h) of the artery's intima via an implanted silver wire. In pentobarbital-anesthetized, open-chest dogs acute myocardial ischemia was determined by a dehydrogenase-dependent staining of the coronary artery perfusion area. Thrombus weight was determined post-mortem. Saline-treated control animals developed coronary thrombosis after 3.1 +/- 0.4 h of stimulation. Thrombus weight was 64 +/- 3.1 mg. Acute infarct volume was 32 +/- 3.1% of total left ventricle, and 53 +/- 6.2% of the coronary artery risk region for infarction. At occlusive thrombosis, blood pressure, ventricular pressure and the LV dP/dtmax fell significantly, whereas heart rate and the end-diastolic filling pressure increased. Severe ST-segment elevation and loss of R wave voltage indicated myocardial ischemia. At 20 min into thrombotic vessel occlusion, 2,000 IU/min SK were infused by way of a Sones-catheter advanced to the thrombus. Coronary thrombosis consistently lysed after 12 +/- 0.7 min of SK infusion, and coronary blood flow as well as hemodynamics were restored. Only minor acute infarction was found indicating viability of ischemic jeopardized myocardium. In another group, the continuous SK-infusion (20 IU/kg/min) concomitant with electrical vessel stimulation prevented coronary thrombosis and acute ischemia, and no significant hemodynamic alterations were noted. These results indicate that intracoronary SK-infusion can lyse acute thrombosis as sequel of electrical stimulation. This prevents development of acute myocardial infarction. Continuous SK-infusion can completely prevent coronary thrombosis in response to intimal injury.
在一个体内犬模型中，通过植入银线对左旋冠状动脉内膜进行电刺激（150微安，直流电，持续6小时）引发血栓形成，研究了冠状动脉内应用链激酶（SK）的溶栓和血流动力学特性。在戊巴比妥麻醉、开胸的犬中，通过对冠状动脉灌注区域进行脱氢酶依赖性染色来确定急性心肌缺血。血栓重量在死后测定。盐水处理的对照动物在刺激3.1±0.4小时后发生冠状动脉血栓形成。血栓重量为64±3.1毫克。急性梗死体积占左心室总体积的32±3.1%，占冠状动脉梗死危险区域的53±6.2%。在闭塞性血栓形成时，血压、心室压力和左心室dP/dtmax显著下降，而心率和舒张末期充盈压力增加。严重的ST段抬高和R波电压降低表明心肌缺血。在血栓性血管闭塞20分钟时，通过推进到血栓部位的Sones导管以2000国际单位/分钟的速度输注SK。输注SK 12±0.7分钟后冠状动脉血栓持续溶解，冠状动脉血流以及血流动力学得以恢复。仅发现轻微的急性梗死，表明缺血危及心肌的存活能力。在另一组中，在血管电刺激的同时持续输注SK（20国际单位/千克/分钟）可预防冠状动脉血栓形成和急性缺血，且未观察到明显的血流动力学改变。这些结果表明冠状动脉内输注SK可溶解电刺激引发的急性血栓形成。这可预防急性心肌梗死的发生。持续输注SK可完全预防因内膜损伤引起的冠状动脉血栓形成。
