The effect of 0.1 mg/kg Verapamil on the extent of the ischemic area following ligation of a branch of the left descending coronary artery was studied in anesthetized open chest dogs. The sum of the ST-segment elevation during the entire period of occlusion in the epicardial ECG was 15 mV in control infarction compared to 9 mV (p smaller than 0.0005) when Verapamil was infused after ligation. Mean flow in the left descending coronary artery was reduced by coronary ligation alone on the average by 23%, but augmented by Verapamil for 5% above pre-occlusion control flow. Corresponding to the rise in the coronary flow and the drop in perfusion pressure under the influence of Verapamil, the increase of left coronary artery resistance induced by coronary occlusion was diminished. The positive effect of Verapamil on the size of myocardial infarction as estimated from the epicardial ST-segment changes is probably not induced by coronary vasodilatation, but by the Ca-antagonizing effect of this drug, as described by other authors.
In 17 unaesthetized dogs several side branches of the left descending coronary artery were ligated. The ST-segment elevation in the epicardial ECG ascended to 22 mV after 5 min and to 19 mV after 20 min. Aortic pressure, left ventricular enddiastolic pressure, heart rate and hemostasiological parameters (thrombin-time, thrombin-coagulase-time, reptilase-time, plasma-fibrinogen, staphylococcal clumping test) did not change significantly. 20 min after the beginning of coronary occlusion, the vessels were reopened. When ST-segment elevation had disappeared, a controlled fibrinolytic therapy (Streptokinase 1.5 Mega I.E. in 30 min, later on 0.75 Mega I.E./h) was induced. When an effective fibrinolysis could be demonstrated by the hemostasiological parameters, the same vessels were occluded again. Now the hemodynamic parameters too did not change significantly, but the ST-segment elevation was significantly diminished for more than 50% compared with simple ligation. A control group, which only got the solvent of the streptokinase, showed the same ST-segment elevation. This effect, induced by streptokinase is ascribed to fibrinogen degradation products and a diminution in the amount of fibrinogen which cause an improvement of microcirculation.
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