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Rat platelets were labeled with indium-111 (111In) and injected into rats whose aortas were subjected to endothelial denudation. A plot of 111In activity vs the number of missing endothelial cells showed a direct correlation between these parameters and it was possible to detect endothelial denudation when approximately 600 cells were removed. These studies also revealed that intact adjacent endothelium from aortas subjected to injury had detectably increased 111In activity compared with endothelium of control, uninjured rats. This activity was not found if 111In-platelets were preincubated with acetylsalicylic acid (1.3 mM) prior to injection and subsequent denudation procedure. To test if 111In platelet activity could be transported to sites distant from the site of injury, a small catheter (PE 50) was passed down the carotid artery so that it reached the aortic arch or inserted via a femoral artery to the iliac-aortic bifurcation. Significant increases in 111In activity were detected in the lower thoracic aorta when the catheter was introduced into the aortic arch but not when the catheter was introduced via the femoral artery. Morphologic evaluation of these sites showed no endothelial cell loss or adhering platelets. These studies suggest that detectable uptake of released platelet products may occur at distal sites of intact endothelium.

Vascular injury: quantification of experimental focal endothelial denudation in rats using indium-111-labeled platelets.