Y. Merhi et al., NEUTROPHIL IMPLICATIONS IN PLATELET DEPOSITION AND VASOCONSTRICTION AFTER DEEP ARTERIAL INJURY BY ANGIOPLASTY IN PIGS, Circulation, 90(2), 1994, pp. 997-1002
Background Experimental studies in vitro suggest that neutrophils can
modulate platelet function and vasomotor responses. In the present stu
dy, the interactions among neutrophils, platelets, and arterial respon
ses to injury in vivo were assessed. Methods and Results The acute thr
ombotic and vasomotor responses of porcine carotid arteries to balloon
injury in vivo were evaluated in three groups of animals: neutropenic
pigs treated (n=11) or not treated (n=12) with aspirin and healthy un
treated control pigs (n=15). Neutropenia was achieved by treatment wit
h cyclophosphamide (50 mg/kg, 4 days before the experiment), which dec
reased circulating leukocyte count by 92% and almost abolished neutrop
hil aggregation to N-formylmethionyl-leucyl-phenylalanine without affe
cting blood platelet count, hematocrit, hemoglobin concentration, or w
hole blood platelet aggregation to ADP. Cr-51 platelet deposition on d
eeply injured and uninjured arterial segments was not statistically in
fluenced by neutrophil depletion, whereas the angiographic vasoconstri
ctive response at the site of endothelial injury distally was signific
antly reduced by 41% from 46.3+/-2.9% in the control group to 27.2+/-4
.1% in the neutropenic group (P<.05). Aspirin treatment in combination
with neutropenia produced a 50% reduction in whole blood platelet agg
regation, resulted in a significant inhibition of platelet deposition
to deeply injured arteries, and decreased vasoconstriction by 66% to 1
5.6+/-3.0% (P<.05 versus control and neutropenic). Conclusions Neutrop
hils can influence the vasoconstrictive response at the site of endoth
elial injury in vivo. In addition to platelets, neutrophil interaction
with the injured vessel wall may be implicated in the pathophysiologi
cal response to arterial injury in vivo.