Thrombolysis in acute experimental myocardial infarction.
Thrombolysis in acute experimental myocardial infarction.
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急性实验性心肌梗死的溶栓。
DOI：
10.1016/s0735-1097(83)80070-9
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发表时间：
1983
影响因子：
24
通讯作者：
W. Schaper
中科院分区：
文献类型：
--
作者：
K. Karsch;M. Hofmann;K. Rentrop;H. Blanke;W. Schaper
冠状动脉内应用链激酶溶栓治疗急性心肌梗死已成为一种新的治疗方法。为了模拟心肌梗死的临床情况，开发了一种新的实验模型，该模型基于由缩窄器产生的高度狭窄部位处的血栓性冠状动脉闭塞。在20只犬中，在左前降支或回旋支冠状动脉处准备两个相距15 mm的结扎。远端结扎闭合后，通过导管直接在近端结扎前注射2 IU凝血酶。撤回导管并闭合近端结扎。闭塞时间1 ~ 6小时。在闭塞后1、2、4和6小时，将链激酶（100，000 IU溶于200 ml盐水溶液）输注至左冠状动脉主干1小时。连续记录血流动力学参数和冠状动脉血流到缺血和正常心肌区。用示踪剂微球测量6次心肌灌注，在闭塞1小时后5分钟、2小时后8分钟、4小时后15分钟和6小时后30分钟，用链激酶恢复血流，并使缺血区域的心肌灌注正常化;无充血发生。梗死面积的死后染色显示，即使在闭塞6小时后，血栓性血管的灌注区仍有超过50%的存活心肌。出血仅在闭塞6小时后发生，并限于内膜下层的坏死中心区域。严重的再灌注心律失常发生后1和2小时的闭塞，似乎是独立的再灌注模式，然而，再灌注后的室颤发作的总次数可能减少后突然和充血性复流。
Lysis of thrombi by intracoronary application of streptokinase has become a new therapeutic approach in patients with acute myocardial infarction. To simulate the clinical situation of myocardial infarction a new experimental model was developed, which was based on a thrombotic coronary occlusion at the site of a high degree stenosis created by a constrictor. In 20 dogs, two ligations 15 mm apart were prepared at the left anterior descending or circumflex coronary artery. After closure of the distal ligation, 2 IU of thrombin was injected through a catheter directly in front of the proximal ligation. The catheter was withdrawn and the proximal ligation was closed. Occlusion time ranged from 1 to 6 hours. At 1, 2, 4 and 6 hours after occlusion, streptokinase was infused for 1 hour (100,000 IU in 200 ml of saline solution) into the left main coronary artery. Hemodynamic variables and coronary blood flow to the ischemic and normal myocardial areas were recorded continuously. Myocardial perfusion was measured six times with tracer microspheres.Reinstatement of blood flow, as well as normalization of myocardial perfusion in the ischemic area, was achieved by streptokinase at 5 minutes after 1 hour of occlusion, 8 minutes after 2 hours, 15 minutes after 4 hours, and 30 minutes after 6 hours; no hyperemic flow occurred. Postmortem staining of infarct size revealed more than 50% of viable myocardium in the perfusion area of the thrombotic vessel even after 6 hours of occlusion. Hemorrhage occurred only after 6 hours of occlusion and was limited to the central area of necrosis in the subendocardial layer. Serious reperfusion arrhythmias occurred only after 1 and 2 hours of occlusion and seemed to be independent of the mode of reperfusion; however, the total number of episodes of ventricular fibrillation after reperfusion was probably decreased compared with that after sudden and hyperemic reflow.
演变中的心肌梗塞的冠状动脉内溶栓。
影响因子：
39.2
作者：
Ganz,W
通讯作者：
Ganz,W