Dynamics and Source of Endothelin-1 and Interleukin-6 Following Coronary Reperfusion in Patients with Acute Myocardial Infarction
| Autor: | Takahiro Imaizumi, Shinhiro Takeda, Jun Nejima, Teruo Takano, Keiji Tanaka, Kaname Kiuchi, Yoshihiko Seino |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Myocardial Infarction Femoral vein Hemodynamics Myocardial Reperfusion Femoral artery medicine.artery Internal medicine medicine Humans Myocardial infarction Coronary sinus Endothelin-1 Interleukin-6 business.industry General Medicine medicine.disease Endothelin 1 Pulmonary artery Cardiology Blood Vessels Female Endothelin receptor business |
| Zdroj: | Journal of Nippon Medical School. 74:131-147 |
| ISSN: | 1347-3409 1345-4676 |
| DOI: | 10.1272/jnms.74.131 |
| Popis: | Objectives: The goals of this study were to determine the source of circulating endothelin‑ 1 (ET‑1 and interleukin‑6 (IL‑6 in acute myocardial infarction (MI and to study the effects of coronary reperfusion (CR on plasma levels of ET‑1 and IL‑6. Methods: We serially measured plasma concentrations of ET‑1 and IL‑6 at different sampling sites before and after CR in patients with acute MI. A femoral vein (FV catheter a Swan‑Ganz catheter and a femoral artery (FA catheter were placed in 25 patients with acute MI who were admitted within 12 hours after onset . For the measurement of ET‑ 1a nd IL‑6 concentrations blood samples from the FV right atrium (RA pulmonary artery (PA and FA were collected before and 1 hour 8 hours and 24 hours after CR therapy. In 5 of the 25 patients blood samples were collected through a coronary sinus (CS catheter. We also assessed the gradient across 3 vascular beds (systemic pulmonary and coronary as indices of the net release of ET‑1 and IL‑6 from those vascular beds. The maximal serum creatine kinase (CK levels were assessed as an index of myocardial necrosis. Results: ET‑1 levels were higher in the FV than in the RA PA or FA. On CR ET‑1 levels peaked after 1 hour and returned to baseline by 24 hours. Calculated net rel ease of ET‑1 from the systemic vascular bed (ET‑1 at FV―ET‑1 at FA was the highest among the 3 vascular beds. Plasma ET‑1 levels correlated with hemodynamic parameters. Plasma IL‑6 levels were similar among different sampling sites whereas calculated net release o fI L‑6 from the coronary vascular bed was the highest among the 3 vascular beds. IL‑6 levels increased throughout 24 hours after coronary reperfusion and closely correlated with maximal CK levels. Conclusions: The present study suggests that in acute MI the major source of ET‑1 maintaining baseline plasma levels is the systemic vascular bed and that the ET‑1 levels presumably reflect the congestion. ET‑1 levels peaked 1 hour after CR. IL‑6 increased for 24 hours after CR. The major source of IL‑6 is the coronary vascular bed. Only a slight correlation was observed between plasma ET‑1 and IL‑6 levels. (J Nippon Med Sch 2007; 74: 131―147 |
| Databáze: | OpenAIRE |
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