VEGF-induced tube formation in vitro and VEGF-induced vascular permeability in animal model. The tube forming activity was analyzed by the tube length of bovine aortic endothelial cells (BAE cells) incubated between type I collagen gels. The expression of VEGFR-1 and VEGFR-2 in BAE cells was assessed by the fluorescence intensity in the binding of FITC-labeled antibodies against these receptors. The effects of dietary n-3 PUFA on susceptibility to VEGF were detected by the vascular leakage in the back skin of male SD rats injected by VEGF. The pretreatment of BAE cells with n-3 PUFA suppressed VEGF-induced tube formation, but among them DPA was the strongest inhibitor of tube formation. However, when b-FGF was substituted for VEGF, the suppressive effect of DPA was abolished. The treatment of BAE cells with EPA and DPA caused the suppression of VEGFR-2 expression in both plastic dish and collagen gel cultures. To confirm the down-regulation of VEGFR-2 by n-3 PUFA, it was examined whether n-3 PUFA intake affected VEGF-induced vascular permeability. Rats, fed on Soy bean oil, Fish oil and DPA- enriched oil for 21 days, were injected with VEGF on back skin and the leakage of dye was measured quantitatively. VEGF- induced vascular permeability was suppressed in both fish oil and DPA-enriched fish oil group, but the inhibitory effect in DPA-enriched fish oil group was stronger than fish oil one. These data indicate that n-3 PUFA, especially DPA, has beneficial effects on VEGF-related diseases through the down-regulation of VEGFR-2. doi:10.1016/j.vph.2006.08.279 B13.26 High flow induces plaque regression in LDLR mice Yves Castier 1 , Guy Leseche 2 , Alain Tedgui 1 , Stephanie Lehoux 1 1 Inserm U689, Paris, France 2 Hospital Bichat, Paris, France Numerous studies in man and in animals support the relation between low or turbulent shear stress and atherosclerotic plaque location. However, little is known regarding the role of shear stress on the progression and composition of pre-established plaques. Hence, we developed a new model of arteriovenous fistula (AVF) in the mouse connecting the right common carotid artery (RCCA) with the jugular vein. LDL receptor knockout mice (n = 43) were placed on a high-fat diet for 12 weeks (wk0– wk12), then divided in three groups: sham, AVF, or RCCA ligature (LIG). Animals were maintained on high-fat for 4 weeks post-surgery. Plaque size and composition was evaluated in the brachiocephalic artery, a lesion-prone site lying immediately upstream of the RCCA, after fixing vessels at physiological pressure. Body weight, blood pressure, and plasma cholesterol levels were equivalent in all groups. RCCA blood flow was increased more than six-fold in AVF compared with shams (4.40 ± 0.10 vs 0.68 ± 0.08 ml/min, respectively), and completely abolished in LIG. In sham animals, atherosclerotic plaque size in the brachiocephalic artery progressed from 117,400 ± 16,400 (wk12) to 134,200 ± 15,100 μm2 (wk16). Amazingly, plaque size was actually reduced by 53% in AVF compared with sham (62,400± 15,100 μm2, p <0.02), whereas it almost tripled in LIG (264,200 ± 36,900 μm2, p< 0.01). Moreover, treatment of mice with sub-pressor doses of the eNOS inhibitor L-NAME completely abolished plaque regression associated with en- hanced flow in AVF (147,300 ±11,400 μm2), whereas it did not alter plaque size in sham. Collagen content and matrix metalloproteinase activity did not vary significantly between groups, though smooth muscle content (verified by α-actin stain) was greater in sham (10.7±2.9%) than in AVF (1.9± 0.7%) or LIG (2.2 ± 1.5%). Hence, we show that blood flow is a critical determinant of both atherosclerotic lesion size and composition in the established plaque. Our data suggest that a favorable local shear environment not only hinders plaque formation and progression, but it may even reverse the atherosclerotic process. doi:10.1016/j.vph.2006.08.280 B13.27 High initial fibrinogen level is a risk factor for no-reperfusion phenomenon among patients with ST segment elevation myocardial infarction treated with percutaneous coronary intervention Jaroslaw Wasilewski, Tadeusz Osadnik, Lech Polonski, Marian Zembala Silesian Centre for Heart Diseases, Zabrze, Poland Introduction: In considerable percentage of patients with myocardial infarction undergoing percutaneous coronary inter- vention, after restoration of the epicardial blood flow in infract related artery, does not come to restoration of blood flow in myocardial microcirculation. With regard to the fact that blood flow in microcirculation depends not only on structural changes in capillaries but also is dependent on blood rheological properties, we decided to estimate the influence of fibrinogen level on the no-reperfusion phenomenon. Methods: We measured fibrinogen level at admission in 105 patients with acute myocardial infarction treated with percuta- neus coronary intervention. Patients, depending on the degree of ST segment normalization in ECG performed in 30 min after the procedure, were divided into two groups “reperfusion” (n = 79) and “no-reperfusion” (n = 26). Results: Fibrinogen levels were higher in “no-reperfusion” group comparing to “reperfusion” group (395.56 ± 144.98 mg/dl vs.523+/-198.02 mg/dl, p = 0.0004), and positively correlated, in a whole study population, with maximal CK-MB level (r = 0.25, p = 0.019) and with duration of infarct pain (r = 0.31, e101 14th IVBM Abstracts