Both platelets and neutrophlls interact with the injured vessel wall and may contribute to thrombosis and vasospasm. The effect of platelets on neutrophil interactions with the vessel wall was studied in normal and thrombocytopenic pigs. "Cr-labeled platelet deposition (xlO') and '"In-labeled neutrophil deposition (xlO3) on undamaged aortic strips with intact endothelium or damaged aortic strips with exposed media were quantified in superfusion flow chambers before and after platelet depletion by specific rabbit antisera. Arterial blood was drawn at a constant flow rate through the superfusion chambers at 37°C. Under basal conditions, platelets did not adhere to the uninjured vessel wall with intact endothelium, whereas neutrophil interaction with the endothelium was low and constant at shear rates of 427, 853, and 1280 s"1and did not change significantly after thrombocytopenia. On exposed aortic media simulating deep arterial injury, platelet deposition increased over these shear rates from 14.0±3.4 to 37.5 ±12.0 (p<.05) to 68.0±9.0, respectively (p<.05). Similarly, neutrophil deposition on the media increased from 48.7±8.7 to 73.7±14J (P<.0S) to 118-3±22.9, respectivelyp) <.O5). Platelet deposition on the media did not occur after thrombocytopenia (80% reduction in platelet count); however, neutrophil deposition persisted, but was less intense and was now independent of shear rates (233 ±S3. at 427 s"1, 18.7±3.2 at 853 s~', and 24.1 ±3.9 at 1280 s~'; not significant). Additionally, after platelet depletion, neutrophil aggregation with iV-fonnyl-methionyl-leucyl-phenylalanlne (2 × 10"* mol/L) in vitro was inhibited. These results indicate that platelets modulate neutrophil deposition on the exposed aortic media. Under thrombocytopenic conditions, a low level of neutrophil deposition can be unmasked in the absence of any platelet deposition. Neutrophils may thus interact directly with the vessel wall to promote vascular changes independent of platelets.