Dear Sir, Several observations indicate that the concentration of fibronectin in plasma is a determinant of platelet thrombus formation. Injured arterioles of mice engineered to have< 2% or 50% normal plasma fibronectin concentration develop less stable platelet thrombi and occlude more slowly than arterioles of mice with normal plasma fibronectin concentration (1, 2). Fibronectin concentration is also a strong determinant of platelet thrombus build-up in the parallel flow chamber assay (3–5). The concentration of fibronectin varies widely in humans, from 230 to 650 µg/ml (6). High concentrations have been associated with venous thromboembolism (7, 8) and with coronary artery disease in some but not all populations (9–12). The latter association suggests that there is genetic interaction between fibronectin concentration in plasma and other determinants of cardiovascular disease. In order to relate studies in mice to observations in humans, we sought evidence for a similarly wide concentration range of plasma fibronectin in various genetic strains of mice. Rabbit antibodies to purified human plasma fibronectin were purified by affinity chromatography on immobilised human fibronectin. These antibodies recognised mouse fibronectin with high titer, and only fibronectin was detected by the antibodies in Western blots of mouse plasma proteins. A portion of the antibodies was labelled with biotin. Fibronectin from mouse plasma was isolated by affinity chromatography on gelatin as previously described (13). The protein was> 95% pure by electrophoresis and used as a standard, assuming a 1 mg/ml solution to have an optical density (280 nm, 1 cm) of 1.3. Pooled citrated plasma from Swiss family mice was purchased (Pel-Freez, Rogers, AK, USA) and served as reference plasma. The reference plasma, antibodies and purified mouse fibronectin standard were used to measure fibronectin concentration in the plasma by three different immunoassays.