Document Detail


Ventilation with "clinically relevant" high tidal volumes does not promote stretch-induced injury in the lungs of healthy mice.
MedLine Citation:
PMID:  22890257     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Ventilator-induced lung injury is a crucial determinant of the outcome of mechanically ventilated patients. Increasing numbers of mouse studies have identified numerous pathways and mediators that are modulated by ventilation, but it is conceptually difficult to reconcile these into a single paradigm. There is substantial variability in tidal volumes used in these studies and no certainty about the pathophysiology that such varied models actually represent. This study was designed to investigate whether ventilation strategies ranging from "very high" to more "clinically relevant" tidal volumes induce similar pathophysiologies in healthy mice or represent distinct entities.
DESIGN: In vivo study.
SETTING: University research laboratory.
SUBJECTS: C57/Bl6 mice.
INTERVENTIONS: Anesthetized mice were ventilated with various tidal volumes up to 40 mL/kg.
MEASUREMENTS AND MAIN RESULTS: Respiratory system compliance and arterial blood gases were used to evaluate physiological variables of injury. Lung wet:dry weight ratio, lavage fluid protein, and cytokines were used to assess pulmonary edema and inflammation. All ventilation strategies induced changes in respiratory system compliance, although the pattern of change was unique for each strategy. Ventilation with 10 mL/kg and 40 mL/kg also induced decreases in arterial PO2 and blood pressure. Any physiological changes induced during the 10, 20, and 30 mL/kg strategies were largely reversed by recruitment maneuvers at the end of the protocol. Markers of pulmonary edema and inflammation indicated that only 40 mL/kg induced substantial increases in both, consistent with development of lung injury.
CONCLUSIONS: Tidal volumes up to 20 mL/kg are unlikely to induce substantial lung overstretch in models using healthy, young mice. Signs of injury/inflammation using such models are likely to result from other factors, particularly alveolar derecruitment and atelectasis. The results of such studies may need to be reevaluated before clinical relevance can be accurately determined.
Authors:
Michael R Wilson; Brijesh V Patel; Masao Takata
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Critical care medicine     Volume:  40     ISSN:  1530-0293     ISO Abbreviation:  Crit. Care Med.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-24     Completed Date:  2012-11-20     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  0355501     Medline TA:  Crit Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2850-7     Citation Subset:  AIM; IM    
Affiliation:
Section of Anaesthetics, Pain Medicine and Intensive Care, Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital, London, United Kingdom. michael.wilson@imperial.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Gas Analysis
Hemodynamics
Inflammation / physiopathology
Male
Mice
Mice, Inbred C57BL
Pulmonary Edema / physiopathology
Respiration, Artificial / adverse effects*,  methods*
Tidal Volume
Time Factors
Ventilator-Induced Lung Injury / physiopathology*
Grant Support
ID/Acronym/Agency:
081208//Wellcome Trust; 092851//Wellcome Trust; 092851//Wellcome Trust
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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