Importance of platelets in neutrophil adhesion and vasoconstriction after deep carotid arterial injury by angioplasty in pigs.

In previous studies we have shown that platelets can support neutrophil adhesion to the injured vessel wall in vitro and that neutrophils contribute to vascular tone regulation after arterial injury in vivo. In this study, we investigated the implication of platelets in neutrophil adhesion and the vasomotor response to arterial injury in vivo. 111In-labeled neutrophil adhesion and angiographic vasoconstriction were quantified after deep carotid arterial injury by balloon angioplasty in normal (n = 8), thrombocytopenic (n = 7), and aspirin-treated (2 mg/kg IV, n = 7) pigs. Thrombocytopenia was produced by a polyclonal antiplatelet serum that depleted circulating platelet count by 84% without influencing neutrophil count. In the control animals, neutrophil adhesion (x 10(4)/cm2) at the site of deep arterial injury averaged 26.8 +/- 4.0 and decreased significantly to 11.5 +/- 2.3 and 11.2 +/- 2.4 in the thrombocytopenic and aspirin groups, respectively. The degree of vasconstriction was also reduced significantly, from 55.5 +/- 3.8% in the control group to 31.4 +/- 6.2% after platelet depletion and to 23.6 +/- 4.5% in the aspirin-treated group. Neutrophil adhesion to intact noninjured adjacent arterial segments was low in all groups and was not affected by the antiplatelet serum or by aspirin. In in vitro superfusion flow chambers, neutrophil adhesion to damaged arterial segments increased in the presence of platelets in a concentration-dependent manner and was not influenced by the antiplatelet serum. This study demonstrates that platelets can modulate neutrophil adhesion to the deeply injured arterial wall and that both elements may influence the degree of postangioplasty vasoconstriction in vivo.