Efecto inmunomodulador del sevoflurano en un modelo experimental de síndrome de distrés respiratorio agudo (ards)

  1. ferrando ortolá, carlos
Dirigida por:
  1. Bruno Camps Vilata Director/a
  2. Marina Soro Domingo Codirector/a

Universidad de defensa: Universitat de València

Fecha de defensa: 30 de junio de 2011

Tribunal:
  1. Carmen-Vicenta Gomar Sancho Presidente/a
  2. Francisco Javier Belda Nacher Secretario/a
  3. Luciano Aguilera Celorrio Vocal
  4. Roque Joaquín Company Teuler Vocal
  5. José Ignacio Gómez Herreras Vocal

Tipo: Tesis

Teseo: 315285 DIALNET

Resumen

BRIEF: The lung inflammatory response and the oxygenation are measured during sedation in ARDS model. The authors demonstrate in 16 pigs with ARDS that sevoflurane, but not propofol, reduces the lung inflammatory response and improves the oxygenation. ABSTRACT Introduction : Acute respiratory distress syndrome (ARDS) is characterized by an activation of the inflammatory cascade. The only treatment that reduces the ARDS mortality is the lung-protective ventilation that requires patient sedation. Most commonly, intravenous drugs are used for ICU sedation. However, inhaled anesthetics may be ideal sedatives for the ICU. Recently, sevoflurane has been shown to modulate the lung inflammatory response in a model of acute lung injury compared to propofol. The goal of this study was to show that, in a model of a ARDS, sevoflurane ameliorates the inflammatory response compared to propofol. Methods: A prospective, randomized and controlled study was carried out in 16 pigs with ARDS. They were randomized to receive sedation with propofol (P) 5-7mg kg-1 h-1 or sevoflurane (S) using the AnaConDa device to obtain an endtidal concentration of 1.5 vol%. Monitoring, lung protective ventilation and anesthetic management were identical for both groups. The ARDS model was made through multiple saline lavage. PaO2/FiO2 and cytokines in bronchoalveolar lavage (BAL) were determined at 10 and 240 min after confirmation of ARDS (PaO2/FiO2 < 200 mmHg). Results: Levels of cytokines in group S were lower than those in group P: IL-1ß (p=0.04) (95% CI 5.1 to 736.6), TNF-¿ (p=0.04) (95% CI 3.9 to 598.8) and IL-6 (p=0.03) (95% CI 19.6 to 587.7). PMN neutrophil count was lower in group S (p=0.007). Additionally, group S showed a better PaO2/FiO2. Conclusion: In this model of ARDS, sevoflurane ameliorates lung inflammatory response and improves oxygenation compared to propofol.