TRANSIENT PLATELET ACCUMULATION IN THE RAT-BRAIN AFTER COMMON CAROTID-ARTERY THROMBOSIS - AN IN-111 LABELED PLATELET STUDY

Background and Purpose: Thromboembolic events are a major cause of isc hemic stroke. To obtain evidence for platelet embolization after cereb rovascular injury, the accumulation of indium-labeled platelets was do cumented after photothrombosis of the rat common carotid artery. Metho ds: Heterologous blood was collected from donor rats, and the isolated platelets were labeled with In-111-tropolone. Labeled platelets were then infused into Wistar rats 30 minutes before right carotid artery t hrombosis. Nonocclusive common carotid artery thrombosis was induced b y a laser-driven rose bengal-mediated photochemical insult to the vasc ular endothelium, and the rats were killed 15 minutes or 3 hours later . Carotid arteries and brains were immediately removed and dissected f or regional radioactivity assessment or sectioned for the autoradiogra phic visualization of platelet emboli. Results: At 15 minutes after th rombosis, the ratio of right-to-left common carotid artery radioactivi ty was significantly elevated compared with control (33+/-12 [mean+/-S EM] versus 0.97+/-0.2). Within individual brain regions, including the frontal and frontoparietal cortices and hippocampus, significant elev ations in right-to-left radioactivity ratios were also documented. Aut oradiographic images revealed multiple foci of In-111-labeled platelet s throughout the thrombosed hemisphere. At the level of the frontal co rtex, bilateral platelet accumulation was seen. Regional counts demons trated significantly increased platelet density within selective corti cal and subcortical regions. In contrast to the 15-minute findings, ri ght-to-left ratios of carotid arteries or brain regional radioactiviti es were not significantly elevated at 3 hours after injury. In additio n, the areal densities of autoradiographically visualized platelets in the 3-hour group were not different from control except in the right frontal cortex. Conclusions: These data demonstrate (1) the acute accu mulation of labeled platelets in downstream vessels after nonocclusive common carotid artery thrombosis, (2) that platelet accumulation is w idespread and also involves contralateral areas, and (3) that platelet accumulation within the thrombosed carotid artery and brain is largel y transient.