Tryptase is involved in the development of early ventilator-induced pulmonary fibrosis in sepsis-induced lung injury

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• 作者：Jes煤s Villar (1) (2) (3)
  Nuria E Cabrera-Ben铆tez (1) (2)
  Francisco Valladares (1) (4)
  Sonia Garc铆a-Hern谩ndez (4)
  脕ngela Ramos-Nuez (1) (2)
  Jos茅 Lu铆s Mart铆n-Barrasa (2)
  Mercedes Muros (1) (5)
  Robert M Kacmarek (6) (7)
  Arthur S Slutsky (3) (8)
  
  1. CIBER de Enfermedades Respiratorias ; Instituto de Salud Carlos III ; Monforte de Lemos 3-5 ; 28029 ; Madrid ; Spain
  2. Multidisciplinary Organ Dysfunction Evaluation Research Network ; Research Unit ; Hospital Universitario Dr. Negrin ; Barranco de la Ballena ; s/n ; Las Palmas de Gran Canaria ; 35010 ; Spain
  3. Keenan Research Center for Biomedical Science ; St. Michael鈥檚 Hospital ; 30 Bond Street ; Toronto ; ON ; M5B 1W8 ; Canada
  4. Department of Anatomy ; Pathology and Histology ; University of La Laguna ; Campus de CC. de la Salud ; 38071 ; Tenerife ; Spain
  5. Department of Clinical Biochemistry ; Hospital Universitario NS de Candelaria ; Ctra. Gral. del Rosario ; 145 ; Santa Cruz de Tenerife ; 38010 ; Spain
  6. Department of Respiratory Care ; Massachusetts General Hospital ; 55 Fruit Street ; Boston ; MA ; 02114 ; USA
  7. Department of Anesthesia ; Harvard University ; 75 Francis Street ; Boston ; MA ; 02115 ; USA
  8. Interdepartmental Division of Critical Care Medicine ; University of Toronto ; 585 University Avenue ; Toronto ; ON ; M5G 2N2 ; Canada
  
• 刊名：Critical Care
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：19
• 期：1
• 全文大小：3,431 KB
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• 刊物主题：Intensive / Critical Care Medicine; Emergency Medicine;
• 出版者：BioMed Central
• ISSN：1364-8535

文摘

Introduction Most patients with sepsis and acute lung injury require mechanical ventilation to improve oxygenation and facilitate organ repair. Mast cells are important in response to infection and resolution of tissue injury. Since tryptase secreted from mast cells has been associated with tissue fibrosis, we hypothesized that tryptase would be involved in the early development of ventilator-induced pulmonary fibrosis in a clinically relevant model of sepsis-induced lung injury. Methods Prospective, randomized, controlled animal study using Sprague-Dawley rats. Sepsis was induced by cecal ligation and perforation. Animals were randomized to spontaneous breathing or two ventilatory strategies for 4 h: protective ventilation with tidal volume (VT) = 6 ml/kg plus 10 cmH2O positive end-expiratory pressure (PEEP) or injurious ventilation with VT = 20 ml/kg plus 2 cmH2O PEEP. Healthy, non-ventilated animals served as non-septic controls. We studied the following end points: histology, serum cytokine levels, hydroxyproline content, tryptase and proteinase-activated receptor-2 (PAR-2) protein level in lung homogenates, and tryptase and PAR-2 immunohistochemical localization in the lungs. Results All septic animals developed acute lung injury. Animals ventilated with high VT had a significant increase of pulmonary fibrosis, hydroxyproline content, tryptase and PAR-2 protein levels compared to septic controls (P Conclusions Mechanical ventilation modified tryptase and PAR-2 in injured lungs. Increased levels of these proteins were associated with development of sepsis and ventilator-induced pulmonary fibrosis early in the course of sepsis-induced lung injury.