Journal article icon

Journal article

Low tidal volume ventilation ameliorates left ventricular dysfunction in mechanically ventilated rats following LPS-induced lung injury

Abstract:
Background: High tidal volume ventilation has shown to cause ventilator-induced lung injury (VILI), possibly contributing to concomitant extrapulmonary organ dysfunction. The present study examined whether left ventricular (LV) function is dependent on tidal volume size and whether this effect is augmented during lipopolysaccharide(LPS)-induced lung injury. Methods: Twenty male Wistar rats were sedated, paralyzed and then randomized in four groups receiving mechanical ventilation with tidal volumes of 6 ml/kg or 19 ml/kg with or without intrapulmonary administration of LPS. A conductance catheter was placed in the left ventricle to generate pressure-volume loops, which were also obtained within a few seconds of vena cava occlusion to obtain relatively load-independent LV systolic and diastolic function parameters. The end-systolic elastance / effective arterial elastance (Ees/Ea) ratio was used as the primary parameter of LV systolic function with the end-diastolic elastance (Eed) as primary LV diastolic function. Results: Ees/Ea decreased over time in rats receiving LPS (p = 0.045) and high tidal volume ventilation (p = 0.007), with a lower Ees/Ea in the rats with high tidal volume ventilation plus LPS compared to the other groups (p < 0.001). Eed increased over time in all groups except for the rats receiving low tidal volume ventilation without LPS (p = 0.223). A significant interaction (p < 0.001) was found between tidal ventilation and LPS for Ees/Ea and Eed, and all rats receiving high tidal volume ventilation plus LPS died before the end of the experiment. Conclusions: Low tidal volume ventilation ameliorated LV systolic and diastolic dysfunction while preventing death following LPS-induced lung injury in mechanically ventilated rats. Our data advocates the use of low tidal volumes, not only to avoid VILI, but to avert ventilator-induced myocardial dysfunction as well
Publication status:
Published
Peer review status:
Peer reviewed

Actions

Access Document

Files:
Publisher copy:
10.1186/s12871-015-0123-8

Authors

More by this author
Role:
Author
ORCID:
0000-0003-3845-1950
More by this author
Role:
Author
ORCID:
0000-0002-7558-9011
More by this author
Role:
Author
ORCID:
0000-0002-3315-2006
More by this author
Role:
Author
ORCID:
0000-0003-2784-1961
More by this author
Institution:
University of Oxford
Role:
Author
ORCID:
0000-0003-3969-7792


Publisher:
BioMed Central
Journal:
BMC Anesthesiology More from this journal
Volume:
15
Issue:
1
Pages:
140-140
Publication date:
2015-10-07
DOI:
EISSN:
1471-2253
ISSN:
1471-2253


Language:
English
Keywords:
Pubs id:
1235042
UUID:
uuid_69ea4608-00c7-41aa-99f5-c3949466f0a3
Local pid:
pubs:1235042
Source identifiers:
W1900218898
Deposit date:
2025-12-06
ARK identifier:
This ORA record was generated from metadata provided by an external service. It has not been edited by the ORA Team.

Terms of use


Views and Downloads






If you are the owner of this record, you can report an update to it here: Report update to this record

TO TOP