Leukocyte/endothelium activation and interactions during femoral percutaneous transluminal angioplasty.
Recent data suggest that leukocyte-endothelium activation/interactions are important for restenosis after percutaneous transluminal angioplasty (PTA). Ten patients with superficial femoral artery occlusive disease (stage Fontaine IIb) were examined after a percutaneous transluminal angioplasty (PTA) versus a preceding aortoangiography (AAG). Blood samples from corresponding femoral arteries and veins were obtained before, immediately after, and 4 hours after each procedure. The authors examined the ex vivo respiratory burst and leukocytic expression of adhesion molecules flowcytometrically, adhesion molecule plasma concentrations, and inflammatory mediators concentrations in plasma and in endotoxin-stimulated whole blood cultures by ELISA, and the leukocyte counts. After PTA, venous plasma concentrations of soluble (s)L-selectin (148.2 +/-14.7%, p<0.05 vs 100% baseline +/- sem), sP-selectin (130.7 +/-6.9%, p<0.01; sE-selectin (117.5 +/-8.3%, p<0.05 vs arterial), sLFA-3 (130.7 +/-15.8%, p<0.05) were increased. Expressions of L-selectin (93.0 +/-5.7%, p<0.05 vs arterial), CD11a (98.8 +/-3.8%, p=0.06), CD18 (96.9 +/-4.0%, p<0.05 vs arterial), and ICAM-1 (89.1 +/-7.7%, p<0.05) on polymorphonuclear neutrophils (PMN), and arteriovenous leukocyte counts (arterial: 103.5 +/-5.4%, venous: 91.1 +/-3.3%, p<0.05) decreased. Venous ex vivo secretions of oxygen radicals (141.4 +/-28.1%, p<0.05 vs AAG), PMN-elastase (173.7 +/-35.7%, p<0.05 vs AAG), and interleukin (IL)-8 (226.5 +/-56.4%, p<0.001; p<0.0001 vs AAG), as well as PMN-elastase (173.7 +/-35.7%, p<0.05 vs AAG) and tumor necrosis factor (TNF)-alpha plasma concentrations (124.1 +/-11.9%, p=0.06) rose. Four hours after PTA, a leukocytosis and exhausted TNF-alpha (69.8 +/-10.4%, p<0.05) and IL-8 secretions (72.4 +/-4.6%, p<0.01) occurred. PTA induced local leukocyte-endothelium activations (stronger ex vivo mediator productions) and interactions (decreased venous leukocyte counts, increased plasma concentrations, and decreased leukocytic expression of adhesion molecules) with the release of inflammatory mediators (higher plasma concentrations and exhaustions after 4 hours).
Lüdemann
J
J
Department of Internal Medicine, Ev. Hospital Königin Elisabeth Herzberge, Herzbergstrasse 79, 10362 Berlin, Germany.
Schulte
K L
KL
Hader
O
O
Brehme
S
S
Volk
H D
HD
Döcke
W D
WD
D000368:Aged; D000792:Angiography; D000800:Angioplasty, Balloon; D001027:Aortography; D001157:Arterial Occlusive Diseases / Q000097:blood / Q000628:therapy; D015815:Cell Adhesion Molecules / Q000097:blood / Q000502:physiology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism*; D004731:Endotoxins / Q000494:pharmacology; D005260:Female; D005263:Femoral Artery / Q000000981:diagnostic imaging / Q000601:surgery*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007962:Leukocytes / Q000187:drug effects* / Q000502:physiology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D010586:Phagocytes / Q000187:drug effects / Q000502:physiology; D015539:Platelet Activation / Q000187:drug effects* / Q000502:physiology*; D016897:Respiratory Burst / Q000187:drug effects; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
D015815:Cell Adhesion Molecules; D004731:Endotoxins; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D013755:Tetradecanoylphorbol Acetate