Ventilation-induced lung injury is associated with an increase in gut permeability

Shock. 2003 Jun;19(6):559-63. doi: 10.1097/01.shk.0000070738.34700.bf.

Abstract

Mechanical ventilation is associated with several harmful effects mainly related to high tidal volumes (Vt). Ventilator-induced lung injury can be responsible for an increased production of inflammatory mediators. We evaluated remote consequences on the gut of lung triggered inflammatory response, neutralizing anti-tumor necrosis factor (TNF) antibody was administered to assess the role of TNF in lung and gut permeability changes. Rats were anesthetized and ventilated for 2 h. A control group (Con: Vt = 10 mL/kg) was compared with a high Vt group (HV: Vt = 30 ml/kg). One microCi of I125-labeled human serum albumin was injected to measure extravascular albumin space. Gut permeability was evaluated by plasma-to-lumen ratio leakage of I125 human serum albumin. Extravascular albumin space increased in the HV group from 446 +/- 50 microL to 2783 +/- 887 microL. Gut index of permeability increased from 5.1 +/- 1.2 to 14.2 +/- 4.9. Anti-TNF antibody prevented both lung and gut increase in permeability. High tidal volume ventilation resulted in an increase in lung edema and gut permeability, antagonism of TNF with neutralizing antibodies abrogated the increase in gut permeability as well as lung edema.

MeSH terms

  • Animals
  • Antibodies / pharmacology*
  • Cell Membrane Permeability / drug effects
  • Cell Membrane Permeability / physiology*
  • Disease Models, Animal
  • Gastrointestinal Motility / drug effects
  • Gastrointestinal Motility / physiology*
  • Oxygen / blood
  • Partial Pressure
  • Rats
  • Rats, Sprague-Dawley
  • Respiration, Artificial / adverse effects*
  • Respiratory Distress Syndrome / etiology*
  • Respiratory Distress Syndrome / physiopathology
  • Tidal Volume
  • Tumor Necrosis Factor-alpha / immunology*

Substances

  • Antibodies
  • Tumor Necrosis Factor-alpha
  • Oxygen