Local blood serotonin and soluble P-selectin levels during percutaneous transluminal balloon angioplasty and primary stenting of the iliac artery

Matsuyama Red Cross Hospital, Matuyama, Ehime, Japan
Surgery (Impact Factor: 3.38). 02/2002; 131(1 Suppl):S256-60. DOI: 10.1067/msy.2002.119798
Source: PubMed


The activation of platelets or leukocytes plays an important role in development of intimal hyperplasia. We investigated whether the local blood serotonin and soluble P-selectin levels changed during endovascular therapy of the iliac artery.
Blood samples were obtained from the iliac artery of 18 lower limbs undergoing percutaneous balloon angioplasty alone (8 limbs, group I) or percutaneous balloon angioplasty and primary stenting (10 limbs, group II). The serotonin levels in platelet-poor plasma were measured in all limbs. In group I the urinary level of the serotonin metabolite 5-hydroxyindoleacetic acid was also measured 24 hours before and 24 hours after the procedures. The soluble P-selectin levels were measured in the 6 patients in group II.
Before angioplasty the mean (+/- SEM) serotonin concentrations were 1.2 +/- 0.2, 1.2 +/- 0.4, and 1.2 +/- 0.3 ng/mL in all cases, group I, and group II, respectively. After angioplasty these values changed to 1.7 +/- 0.4 (P =.0750), 1.2 +/- 0.4 (P =.8001), and 2.1 +/- 0.6 ng/mL (P =.0529), respectively. In group I urinary 5-hydroxyindoleacetic acid concentrations 24 hours before and 24 hours after the procedures were 0.0026 +/- 0.0004 and 0.0031 +/- 0.0006 mg/mg creatinine, respectively (P =.2566). In group II the soluble P-selectin levels significantly increased after intervention, from 26.0 +/- 5.7 to 33.9 +/- 5.3 ng/mL (P =.0296).
Although the serotonin levels did not change significantly, the soluble P-selectin levels increased significantly after intervention. Leukocyte activation may therefore contribute to the progression of restenosis after peripheral endovascular therapy.

2 Reads
  • [Show abstract] [Hide abstract]
    ABSTRACT: Intravascular stent as a foreign body exhibits obvious reaction following implantation, such as activation of coagulation system and elevation of serum C-reactive protein, inflammatory marker. After platelet is activated, P-selectin binds to the glycoprotein ligand 1 expressed on leukocyte, and forms congeries on the leukocyte. In addition, interleukin-1β, interleukin-6 and tumor necrosis factor-α are greatly secreted. The two factors are main reasons for restenosis following stent implantation. Studies on spiral CT angiography and transcranial Doppler sonography are important.
    No preview · Article · Oct 2008 · Journal of Clinical Rehabilitative Tissue Engineering Research
  • [Show abstract] [Hide abstract]
    ABSTRACT: The reaction process is significant after implantation of cardiovascular stent, with manifestations of the activation of blood coagulation system and dramatically increasing of inflammatory markers serum C-reactive protein. The activated platelet plays an important role in the thrombosis and in-stent restenosis following stent implantation, which can be inhabited by regular anticoagulation therapy and anti-platelet therapy. As external stimulants, firstly, the implanted stent results in platelet aggregation and activation on the surface of stent, secretes various cell factors, such as interleukin-1, interleukin-6, and tumor necrosis factor α, which lead to thrombosis, followed by inflammatory reaction, and proliferative response of smooth muscle cells, eventually lead to arterial remodeling and in-stent restenosis. Accordingly, it is important to prevent intravascular restenosis by recognizing the coagulation system and changes of cell factors.
    No preview · Article · Apr 2009 · Journal of Clinical Rehabilitative Tissue Engineering Research
  • [Show abstract] [Hide abstract]
    ABSTRACT: Intravascular stent as a foreign body induces platelet-monocyte aggregation following implantation, mediates various actions of monocyte, induces monocyte to express tissue factors, promotes fibrin sedimentation at injury site, and accelerates inflammatory reaction of vessel wall injury. In addition, it stimulates platelet aggregation on the stent, activates platelet system and coagulation system, resulting thrombosis. Smooth muscle cells migration to injury site, neointima hyperplasia, and vessel wall reconstruction cause in-stent restenosis. The influential factors that induce restenosis include type of stent, original diseases of the host, stenosis severity before stenting and residual stenosis length after stenting. Inhibition of tunica intima hyperplasia or improvement of neointima as well as vessel wall reconstruction could effectively prevent restenosis.
    No preview · Article · May 2009 · Journal of Clinical Rehabilitative Tissue Engineering Research
Show more