INCREASE OF NEUTROPHIL ADHESION AND VASOCONSTRICTION WITH PLATELET DEPOSITION AFTER DEEP ARTERIAL INJURY BY ANGIOPLASTY

Physiopathologic events after arterial injury are largely influenced b y blood element reactions with the injured surface. To determine acute arterial reactivity to injury, simultaneous chromium 51-labeled plate let deposition and indium 111-labeled neutrophil adhesion were quantif ied at the site of different degrees of carotid arterial injury by bal loon dilatation in 21 normal pigs. The degree of vasoconstriction dist ally to the dilated areas was also quantified angiographically. Arteri es were classified histologically as (1) uninjured with intact endothe lium; (2) mildly injured with endothelial desquamation; or (3) deeply injured with lesions extending beyond internal elastic lamina, exposin g the media. We found that, compared to mild injury, deep injury was a ssociated with greater platelet deposition (38.2 +/- 5.7 X 10(6)/cm(2) vs 7.8 +/- 0.9 X 10(6)/cm(2); p < 0.05), neutrophil adhesion (30.6 +/ - 4.1 X 10(4)/cm(2) vs 10.2 +/- 2.9 X 10(4)/cm(2); p < 0.05), and vaso constrictive response (45.5% +/- 3.2% vs 26.7% +/- 2.8%; p < 0.05). Al though distally to both types of injuries, noninjured arterial segment s with intact endothelium were thromboresistant to platelet deposition , neutrophil adhesion to intact endothelium was much higher after deep injury (2.2 +/- 0.4 x 10(4)/cm(2)) compared to mild injury (0.36 +/- 0.1 X 10(4)/cm(2); p < 0.05). Like platelet deposition, neutrophil adh esion is influenced by the severity of arterial injury; both may there fore be implicated in thrombogenesis and vascular responsiveness after arterial injury in vivo.