An animal model was developed to study arterial thrombosis and determine if animals infected with Helicobacter pylori behave differently after induction of direct damage to blood vessels. Twenty-one C56/BL6 mice inoculated with the "Sydney strain" of H. pylori and 19 uninfected animals were kept for 1 year before testing. Vascular lesions were induced to mesenteric arterioles (15-25 microm diameter) by Argon laser. The dynamic course of thrombus formation was continuously monitored by a video camera for 10 min. Three parameters were assessed: (1) the number of laser pulses required to induce thrombus formation, (2) the number of platelet emboli removed by the blood flow and, (3) the duration of embolization. Additionally, blood was tested for platelet aggregation, fibrinogen, and cell count. Of the parameters measured, statistical differences between infected and uninfected mice concerned the number of emboli formed (6.00+/-2.18 infected vs. 3.89+/-1.37 non-infected, p=.0006) and the duration of embolization (2.41+/-0.73 min infected vs. 1.47+/-0.61 min non-infected p>.0001). A significant difference was also found in the fibrinogen levels between infected and uninfected mice. Chronic infection of mice with H. pylori leads to increased platelet embolization after damage to arterioles. These results are in favor of the possible involvement of H. pylori infection in the acute phase of coronary heart disease (CHD).