Leukocyte/Endothelium Activation and Interactions During Femoral Percutaneous Transluminal Angioplasty

Abstract

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).

Renal angioplasty causes a rapid transient increase in inflammatory biomarkers, but reduced levels of interleukin-6 and endothelin-1 1 month after intervention

“…TNFa responses have been evaluated after femoral percutaneous transluminal angioplasty [26,27] and an immediate increase followed by an exhaustion of TNFa levels 4 h after the intervention is known to occur. Such a transient increase cannot be excluded in our patients, as we did not collect blood samples until the day after intervention.…”

“…Angioplasty in coronary [16][17][18][19][20][21][22][23][24] and lower limb [25][26][27][28] arteries induces local and systemic inflammatory responses, with increasing levels of hs-CRP, leukocyte and platelet activation, and significant increases in neutrophil and monocyte counts. In a small study of patients with RAS followed up for only 24 h after PTRA, renal artery stent implantation has been shown to trigger inflammatory responses with increased plasma hs-CRP and IL-6 levels [29].…”

Standardized immune monitoring for the prediction of infections after cardiopulmonary bypass surgery in risk patients

“…Applying the Quantibrite™ principle in flow cytometry, we quantified the monocytic and granulocytic surface expression of CD64 (26, 27), CD11b (28, 29), and CD71 (30) as markers of “inflammation‐triggered” phagocytes, as well as monocytic CD86 (31) and HLA‐DR (15–18, 31) as markers of antigen‐presenting capacity (APC). In addition, the functional inflammatory capacity of monocytes and granulocytes were tested by the ex vivo release of LPS‐induced TNF‐α (15, 32, 33) and Phorbol‐Myristate‐Acetate (PMA)‐induced elastase (7, 34–36), respectively. Furthermore, we quantified the IL‐10 plasma levels at day 1 after CPB surgery using a novel semiautomatic measurement, as IL‐10 is a key immunomodulatory cytokine that is involved in a number of anti‐inflammatory effects, including deactivation of monocytes.…”

Colchicine Inhibits Intimal Hyperplasia and Leukocyte VEGF Expression in Dogs

“…Roque et al reported margination of leukocytes, predominantly neutrophils as early as one hour after femoral artery denudation injury and that this margination of leukocytes, in the absence of an endothelium, is mediated by interactions between leukocyte receptors and adhesion molecules on the denuded surface [5]. On activation and recruitment to the areas of injury, leukocytes degranulate and release cytokines (e.g., VEGF) and inflammatory mediators such as tumor necrosis factor-alpha, interleukin-8, and oxygen radicals capable of promoting additional tissue injury [5][6][7][8]. Several studies demonstrated a direct correlation between the magnitude of inflammatory cell accumulation and the magnitude of subsequent neointimal mass and that inhibition of inflammatory cell accumulation resulted in reduced neointimal mass [4,31,[33][34][35].…”

“…Moreover, vessel wall injury induces activation of leukocytes with upregulation of cell adhesion molecule expression [4]. Activated leukocytes bind to the denuded surface and degranulate releasing vascular endothelial growth factor (VEGF), a potent inducer of SMCs proliferation and migration [5][6][7][8]. Smooth muscle cell proliferation and migration play a major role in the genesis of intimal hyperplasia after angioplasty or vascular injury.…”