title: Mechanical ventilation may increase susceptibility to the development of bacteremia.
abstract: OBJECTIVE
  We examined the hypothesis that mechanical ventilation with a potentially injurious strategy would predispose animals to the detrimental effects of subsequent instillation of bacteria.
  
  
  METHODS
  Interventional animal study.
  
  
  METHODS
  A university hospital research laboratory.
  
  
  METHODS
  Fifty Sprague-Dawley male rats.
  
  
  METHODS
  Rats were anesthetized and randomized to receive a protective (tidal volume 7 mL/kg, positive end-expiratory pressure 5 cm H(2)O, n = 25) or an injurious ventilatory strategy (tidal volume 21 mL/kg, zero positive end-expiratory pressure, n = 25). Hemodynamics were similar during the 1-hr ventilation period in the two groups. Animals were then disconnected from the ventilator and Pseudomonas aeruginosa was instilled intratracheally before extubation. Thereafter, animals breathed spontaneously; mortality rate was assessed up to 48 hrs, at which time the animals were killed.
  
  
  RESULTS
  The 48-hr mortality rate was 28% in the protective group and 40% in the injurious group (p = not significant). A positive bacterial culture from the lung was obtained in 56% of the surviving rats in the low tidal volume group and 67% in the high tidal volume group (p =.059). A positive blood bacterial culture was found in 11% of the low tidal volume group and 33% in the high tidal volume group (p <.05). The absolute bacterial count in the blood was lower in the low tidal volume group compared with the high tidal volume group (p <.05). Concentrations of blood tumor necrosis factor-alpha and macrophage inflammatory protein-2, and lung macrophage inflammatory protein-2 at 48 hrs were significantly higher in the low tidal volume group than in the high tidal volume group.
  
  
  CONCLUSIONS
  An injurious ventilatory strategy predisposes animals to subsequent bacteremia associated with an impaired host defense reflected by cytokine response.
authors.affiliation: Department of Medicine, Mackay Memorial Hospital, Taiwan.
authors.forename: Chang-Yi
authors.initials: CY
authors.lastname: Lin
authors.forename: Haibo
authors.initials: H
authors.lastname: Zhang
authors.forename: Kuo-Chen
authors.initials: KC
authors.lastname: Cheng
authors.forename: Arthur S
authors.initials: AS
authors.lastname: Slutsky
mesh_terms: D000403:Airway Resistance; D000818:Animals; D016470:Bacteremia / Q000097:blood / Q000209:etiology* / Q000276:immunology / Q000401:mortality; D001784:Blood Gas Analysis; D001794:Blood Pressure; D015984:Causality; D054426:Chemokine CXCL2; D003428:Cross Infection / Q000097:blood / Q000209:etiology* / Q000276:immunology / Q000401:mortality; D004195:Disease Models, Animal; D004198:Disease Susceptibility; D006339:Heart Rate; D008168:Lung / Q000737:chemistry; D008297:Male; D015846:Monokines / Q000032:analysis / Q000097:blood; D011175:Positive-Pressure Respiration / Q000009:adverse effects* / Q000379:methods; D011552:Pseudomonas Infections / Q000097:blood / Q000209:etiology* / Q000276:immunology / Q000401:mortality; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012121:Respiration, Artificial / Q000009:adverse effects* / Q000379:methods; D013990:Tidal Volume; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D054426:Chemokine CXCL2; D015846:Monokines; D014409:Tumor Necrosis Factor-alpha