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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1995;15:128-132.)
© 1995 American Heart Association, Inc.

Articles

Collagen-Induced Thrombus Formation in Flowing Nonanticoagulated Human Blood From Habitual Smokers and Nonsmoking Patients With Severe Peripheral Atherosclerotic Disease

Helge E. Roald; Torstein Lyberg; Henrik Dedichen; Marjo Hamers; Peter Kierulf; Åse-Brit Westvik; Kjell S. Sakariassen

From the Faculty of Medicine, University of Oslo (H.E.R.); Research Forum, Ullevaal University Hospital (T.L.); the Department of Surgery, Ullevaal University Hospital (H.D.); Nycomed Bioreg AS (M.H., K.S.S.); the Clinical Chemistry Department, Ullevaal University Hospital (P.K., A.-B.W.); and the Department of Biology, Division of General Physiology, University of Oslo (K.S.S.), Oslo, Norway.

Correspondence to Dr Helge Einar Roald, University of Oslo, c/o Nycomed Bioreg AS, Gaustadalléen 21, 0371 Oslo, Norway.

Abstract The objective of the present study was to investigate collagen-induced platelet thrombus formation at arterial blood flow conditions in nonanticoagulated blood from habitual smokers and from nonsmoking patients with severe peripheral atherosclerotic disease. Collagen-induced thrombogenesis was elicited in native blood drawn directly from an antecubital vein over immobilized type III collagen fibrils coated on a coverslip positioned in a parallel-plate perfusion chamber. The wall shear rates at the collagen surface were comparable to those encountered in medium-sized (650 s^-1) and moderately stenosed (2600 s^-1) arteries. Thrombus formation in blood from habitual smokers after 10 hours of smoking abstinence appeared to be not different from thrombus formation in blood from healthy nonsmokers. However, immediately after a cigarette had been smoked, thrombus volume in blood from the same individuals was increased twofold at the highest shear rate (P<.05). Thus, the thrombotic response was temporarily upregulated after smoking. Thrombus formation in blood from nonsmoking patients with severe peripheral atherosclerotic disease was neither enhanced nor decreased but was within the range of the nonsmoking control subjects. However, fibrinopeptide A generation after 4 minutes of perfusion at 2600 s^-1 was higher in blood from the atherosclerotic patients (P<.05) and associated with a higher plasma fibrinogen level (P<.005). Thus, signs of changed platelet reactivity in flowing nonanticoagulated blood were encountered only in the habitual smokers immediately after they had smoked a cigarette.

Key Words: cigarette smoking • intermittent claudication • peripheral arterial disease • arterial blood flow • thrombus formation

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