T. Siminiak et al., PLASMA-MEDIATED NEUTROPHIL ACTIVATION DURING ACUTE MYOCARDIAL-INFARCTION - ROLE OF PLATELET-ACTIVATING-FACTOR, Clinical science, 89(2), 1995, pp. 171-176
1. Polymorphonuclear neutrophils are involved in the development of my
ocardial injury during ischaemia through the release of free oxygen ra
dicals and by adhesion of activated polymorphonuclear neutrophils to e
ndothelium, resulting in plugging of coronary capillaries. Polymorphon
uclear neutrophil activation may be a result of contact with ligands e
xpressed by endothelial cells and/or a response to soluble stimuli rel
eased from ischaemic tissue to the plasma. 2. To investigate this we s
tudied plasma-mediated polymorphonuclear neutrophil activation in vitr
o using plasma samples collected from 14 patients with acute myocardia
l infarction at time of admission and 6 h and 1, 2, 5 and 7 days later
. Plasma samples were incubated with washed polymorphonuclear neutroph
ils isolated from healthy donors. Expression of adhesion molecules CD1
8/CD11b integrin and L-selectin (Leu-8) were measured by flow cytometr
y and superoxide anion production in polymorphonuclear neutrophils was
measured by chemiluminescence. 3. Plasma samples obtained 66 and 1 da
y after admission were capable of inducing CD18/CD11b antigen expressi
on, superoxide anion production and L-selectin shedding in the washed
polymorphonuclear neutrophils, and this effect was significant when co
mpared with plasma taken at 5 and 7 days after admission. 4. The plasm
a-mediated polymorphonuclear neutrophil stimulation was prevented when
the PMN were pretreated antagonists activating factor concentrations
detected in the plasma samples were not higher than those detected in
plasma from healthy subjects. 5. These findings suggest that during ac
ute myocardial infarction peripheral plasma contains soluble stimuli c
apable of inducing polymorphonuclear neutrophil integrin expression, L
-selectin shedding and oxygen free radical production and that platele
t-activating factor appears to act as an autocrine polymorphonuclear n
eutrophil stimulus.