title: Mechanical ventilation with high tidal volumes attenuates myocardial dysfunction by decreasing cardiac edema in a rat model of LPS-induced peritonitis.
abstract: BACKGROUND
  Injurious mechanical ventilation (MV) may augment organ injury remote from the lungs. During sepsis, myocardial dysfunction is common and increased endothelial activation and permeability can cause myocardial edema, which may, among other factors, hamper myocardial function. We investigated the effects of MV with injuriously high tidal volumes on the myocardium in an animal model of sepsis.
  
  
  METHODS
  Normal rats and intraperitoneal (i.p.) lipopolysaccharide (LPS)-treated rats were ventilated with low (6 ml/kg) and high (19 ml/kg) tidal volumes (Vt) under general anesthesia. Non-ventilated animals served as controls. Mean arterial pressure (MAP), central venous pressure (CVP), cardiac output (CO) and pulmonary plateau pressure (Pplat) were measured. Ex vivo myocardial function was measured in isolated Langendorff-perfused hearts. Cardiac expression of endothelial vascular cell adhesion molecule (VCAM)-1 and edema were measured to evaluate endothelial inflammation and leakage.
  
  
  RESULTS
  MAP decreased after LPS-treatment and Vt-dependently, both independent of each other and with interaction. MV Vt-dependently increased CVP and Pplat and decreased CO. LPS-induced peritonitis decreased myocardial function ex vivo but MV attenuated systolic dysfunction Vt-dependently. Cardiac endothelial VCAM-1 expression was increased by LPS treatment independent of MV. Cardiac edema was lowered Vt-dependently by MV, particularly after LPS, and correlated inversely with systolic myocardial function parameters ex vivo.
  
  
  CONCLUSIONS
  MV attenuated LPS-induced systolic myocardial dysfunction in a Vt-dependent manner. This was associated with a reduction in cardiac edema following a lower transmural coronary venous outflow pressure during LPS-induced coronary inflammation.
authors.affiliation: Department of Pediatric Intensive Care, VU university medical center, Amsterdam, The Netherlands. l.smeding@vumc.nl
authors.forename: Lonneke
authors.initials: L
authors.lastname: Smeding
authors.forename: Frans B
authors.initials: FB
authors.lastname: Plötz
authors.forename: Regis R
authors.initials: RR
authors.lastname: Lamberts
authors.forename: Willem J
authors.initials: WJ
authors.lastname: van der Laarse
authors.forename: Martin C J
authors.initials: MC
authors.lastname: Kneyber
authors.forename: A B Johan
authors.initials: AB
authors.lastname: Groeneveld
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D004489:Edema, Cardiac / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control*; D006321:Heart / Q000503:physiopathology*; D007274:Injections, Intraperitoneal; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000009:adverse effects*; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D023421:Models, Animal; D010538:Peritonitis / Q000150:complications* / Q000209:etiology / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D012121:Respiration, Artificial / Q000379:methods*; D013990:Tidal Volume / Q000502:physiology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D019010:Vascular Cell Adhesion Molecule-1