[Improvement of flow properties using Arwin in acute experimental infarct].
Reduction of blood viscosity by arwin in the acute experimental infarction. The effect of 1 unit/kg arwin on the extent of the ischemic area following ligation of a branch of the left descending coronary artery (LAD) was studied in 13 anesthetized open-chest dogs. 10 min infusion of Arwin veginning simultaneously with coronary occlusion lead to a decrease in plasma fibrinogen concentration by 69% 60 min after the end of the infusion, whereas in the control group (NaCl-infusion, 13 dogs) no equivalent decrease occurred. The average ST-segment elevation (ST) and the number of sites exhibiting ST-segment elevation (NST) in the epicardial Ecg were 9 mV and 5.0 15 min after the end of the infusion (25 min after coronary occlusion) in the Arwin-treated group and 11 mV resp. 5.9 in the control group. In the following 105 min no alteration in the electrocardiographic evidence of infarction occurred in both groups. 15 min reperfusion (after release of coronary ligation) decreased the ischemic injury in both groups significantly: arwin -group ST 4.1 mV, NST 3.0, control 3.9 mV resp. 3.5. During coronary occlusion ST-elevation was significantly less in borderline areas than in the center of the infarction, a reduction of the ischemic injury by arwin in these different zones, however, could also not be established. Hemodynamic alterations were similar in both groups. Systolic, mean and diastolic aortic pressure, left ventricular systolic pressure and heart rate remained nearly constant during 130 min of coronary occlusion, left ventricular dp/dtmax declined by 17%. 25 min after occlusion of the branch coronary flow in the LAD decreased by 38%, after 130 min by 48%. After 15 min reperfusion the reactive hyperemic response had declined to preocclusion levels. A statistically significant difference in the occurence of reperfusion arrhythmias between the arwin -treated group (25%) and control group (39%) could not be evaluated. There was no evidence that a decrease in blood viscosity produced by lowering of fibrinogen concentration concomitantly with coronary occlusion could reduce electrocardiographic assessment of myocardial injury. Conversely, the effects of arwin on impending infarction and severe angina pectoris cannot be predicted from these results. An increase in infarct size, however, which could have occurred after infusion of arwin leading to microembolization by fibrinogen degradation products was never observed.
D000787:Angina Pectoris / Q000503:physiopathology; D000818:Animals; D000925:Anticoagulants; D001794:Blood Pressure; D001809:Blood Viscosity / Q000187:drug effects*; D004285:Dogs; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006339:Heart Rate; D008026:Ligation; D008297:Male; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000503:physiopathology; D012911:Snakes; D014688:Venoms / Q000494:pharmacology*
D000925:Anticoagulants; D014688:Venoms; D005340:Fibrinogen
Verbesserung der Fliesseigenschaften mit Arwin beim akuten experimentellen Infarkt