Y. Merhi et al., IMPORTANCE OF PLATELETS IN NEUTROPHIL ADHESION AND VASOCONSTRICTION AFTER DEEP CAROTID ARTERIAL INJURY BY ANGIOPLASTY IN PIGS, Arteriosclerosis, thrombosis, and vascular biology, 17(6), 1997, pp. 1185-1191
In previous studies we have shown that platelets can support neutrophi
l adhesion to the injured vessel wall in vitro and that neutrophils co
ntribute to vascular tone regulation after arterial injury in vivo. In
this study, we investigated the implication of platelets in neutrophi
l adhesion and the vasomotor response to arterial injury in vivo. In-1
11-labeled neutrophil adhesion and angiographic vasoconstriction were
quantified after deep carotid arterial injury by balloon angioplasty i
n normal (n=8), thrombocytopenic (n=7), and aspirin-treated (2 mg/kg I
V, n=7) pigs. Thrombocytopenia was produced by a polyclonal antiplatel
et serum that depleted circulating platelet count by 84% without influ
encing neutrophil count. In the control animals, neutrophil adhesion (
x 10(4)/cm(2)) 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 vaso
constriction 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 no
ninjured adjacent arterial segments was low in all groups and was not
affected by the antiplatelet serum or by aspirin. In in vitro superfus
ion flow chambers, neutrophil adhesion to damaged arterial segments in
creased in the presence of platelets in a concentration-dependent mann
er and was not influenced by the antiplatelet serum. This study demons
trates that platelets can modulate neutrophil adhesion to the deeply i
njured arterial wall and that both elements may influence the degree o
f postangioplasty vasoconstriction in vivo.