NEUTROPHIL IMPLICATIONS IN PLATELET DEPOSITION AND VASOCONSTRICTION AFTER DEEP ARTERIAL INJURY BY ANGIOPLASTY IN PIGS

Citation
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
Citations number
33
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
90
Issue
2
Year of publication
1994
Pages
997 - 1002
Database
ISI
SICI code
0009-7322(1994)90:2<997:NIIPDA>2.0.ZU;2-5
Abstract
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.