Increase of neutrophil adhesion and vasoconstriction with platelet deposition after deep arterial injury by angioplasty

Physiopathologic events after arterial injury are largely influenced by blood element reactions with the injured surface. To determine acute arterial reactivity to injury, simultaneous chromium 51-labeled platelet deposition and indium 111-labeled neutrophil adhesion were quantified at the site of different degrees of carotid arterial injury by balloon dilatation in 21 normal pigs. The degree of vasoconstriction distally to the dilated areas was also quantified angiographically. Arteries were classified histologically as (1) uninjured with intact endothelium; (2) mildly injured with endothelial desquamation; or (3) deeply injured with lesions extending beyond internal elastic lamina, exposing the media. We found that, compared to mild injury, deep injury was associated with greater platelet deposition (38.2 ± 5.7 × 106/cm2 vs 7.8 ± 0.9 × 106/cm2; p < 0.05), neutrophil adhesion (30.6 ± 4.1 × 104/cm2 vs 10.2 ± 2.9 × 104/cm2; p < 0.05), and vasoconstrictive response (45.5% ± 3.2% vs 26.7% ± 2.8%; p < 0.05). Although distally to both types of injuries, noninjured arterial segments with intact endothelium were thromboresistant to platelet deposition, neutrophil adhesion to intact endothelium was much higher after deep injury (2.2 ± 0.4 × 104/cm2) compared to mild injury (0.36 ± 0.1 × 104/cm2; p < 0.05). Like platelet deposition, neutrophil adhesion is influenced by the severity of arterial injury; both may therefore be implicated in thrombogenesis and vascular responsiveness after arterial injury in vivo.