title: Treatment of acute myocardial infarction with streptokinase does not appear to modulate circulating neutrophil function.
abstract: The administration of thrombolytic therapy is the most common method of achieving patency of the occluded coronary artery in patients with acute myocardial infarction (AMI). However, thrombolytic agents and the byproducts of fibrinolysis have the potential to affect neutrophil activation and thus function, thereby augmenting myocardial damage further. This study assessed the effect of streptokinase administration on the function of circulating neutrophils in patients with AMI. For this neutrophil adherence to human umbilical vein endothelial cells, homotypic neutrophil aggregation, and CD11b and L-selectin expression on the neutrophil membrane prior to and 1 h and 6 h after thrombolytic therapy was monitored. The study population included patients with AMI who received aspirin and streptokinase, and healthy laboratory workers who received aspirin only; all subjects acted as their own controls. Circulating fibrin degradation products and white cells were markedly raised following administration of streptokinase. No significant differences in neutrophil adherence to endothelium, homotypic neutrophil interactions, and CD11b or L-selectin expression were demonstrated between neutrophils, either pre- or post-thrombolytic therapy in the infarct group, or between neutrophils from the infarct group and from the control group. It was concluded that streptokinase produces an abrupt neutrophil leukocytosis together with a marked increase in circulating levels of fibrin degradation products. The assay systems used were unable to show significant sequential changes in circulating neutrophil adhesion and L-selectin or CD11b expression in patients with AMI following thrombolytic therapy or when these patients were compared with controls.
authors.affiliation: Department of Medicine, University of Cape Town, South Africa.
authors.forename: S A
authors.initials: SA
authors.lastname: Adams
authors.forename: S P
authors.initials: SP
authors.lastname: Froese
authors.forename: B K
authors.initials: BK
authors.lastname: Green
authors.forename: P J
authors.initials: PJ
authors.lastname: Commerford
authors.forename: R E
authors.initials: RE
authors.lastname: Kirsch
authors.forename: E G
authors.initials: EG
authors.lastname: Shephard
authors.forename: S C
authors.initials: SC
authors.lastname: Robson
mesh_terms: D018821:CD18 Antigens / Q000097:blood; D002448:Cell Adhesion / Q000187:drug effects; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D019041:L-Selectin / Q000097:blood; D016177:Macrophage-1 Antigen / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D018375:Neutrophil Activation; D009504:Neutrophils / Q000187:drug effects*; D013300:Streptokinase / Q000627:therapeutic use*; D015912:Thrombolytic Therapy
chemical_list: D018821:CD18 Antigens; D005338:Fibrin Fibrinogen Degradation Products; D005343:Fibrinolytic Agents; D016177:Macrophage-1 Antigen; D019041:L-Selectin; D013300:Streptokinase