Document Detail


Perivascular fluid cuffs decrease lung compliance by increasing tissue resistance.
MedLine Citation:
PMID:  20400904     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Lung inflammation causes perivascular fluid cuffs to form around extra-alveolar blood vessels; however, the physiologic consequences of such cuffs remain poorly understood. Herein, we tested the hypothesis that perivascular fluid cuffs, without concomitant alveolar edema, are sufficient to decrease lung compliance.
DESIGN: Prospective, randomized, controlled study.
SETTING: Research laboratory.
SUBJECTS: One hundred twenty male CD40 rats.
INTERVENTIONS: To test this hypothesis, the plant alkaloid thapsigargin was used to activate store-operated calcium entry and increase cytosolic calcium in endothelium. Thapsigargin was infused into a central venous catheter of intact, sedated, and mechanically ventilated rats.
MEASUREMENTS: Static and dynamic lung mechanics and hemodynamics were measured continuously.
MAIN RESULTS: Thapsigargin produced perivascular fluid cuffs along extra-alveolar vessels but did not cause alveolar flooding or blood gas abnormalities. Lung compliance dose-dependently decreased after thapsigargin infusion, attributable to an increase in tissue resistance that was attributed to increased tissue damping and tissue elastance. Airway resistance was not changed. Neither central venous pressure nor left ventricular end diastolic pressure was altered by thapsigargin. Heart rate did not change, although thapsigargin decreased left ventricular systolic function sufficient to reduce cardiac output by 50%. Infusion of the type 4 phosphodiesterase inhibitor, rolipram, prevented thapsigargin from inducing perivascular cuffs and decreasing lung compliance. Rolipram also normalized pressure over time and corrected the deficit in cardiac output.
CONCLUSIONS: Our findings resolve for the first time that perivascular cuff formation negatively impacts mechanical coupling between the bronchovascular bundle and the lung parenchyma, decreasing lung compliance without impacting central venous pressure.
Authors:
Kevin Lowe; Diego F Alvarez; Judy A King; Troy Stevens
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Critical care medicine     Volume:  38     ISSN:  1530-0293     ISO Abbreviation:  Crit. Care Med.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-26     Completed Date:  2010-07-15     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  0355501     Medline TA:  Crit Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1458-66     Citation Subset:  AIM; IM    
Affiliation:
Department of Surgery, Center for Lung Biology, University of South Alabama, Mobile, Alabama, USA.
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MeSH Terms
Descriptor/Qualifier:
Acute Lung Injury / etiology*,  metabolism,  pathology
Animals
Capillary Permeability / drug effects,  physiology*
Enzyme Inhibitors / pharmacology
Extravascular Lung Water / drug effects,  physiology*
Lung Compliance / drug effects,  physiology*
Male
Phosphodiesterase Inhibitors / pharmacology
Pulmonary Edema / etiology*,  metabolism,  pathology
Rats
Respiratory Mechanics / drug effects,  physiology*
Rolipram / pharmacology
Thapsigargin / pharmacology
Vascular Resistance / drug effects,  physiology
Grant Support
ID/Acronym/Agency:
HL60024/HL/NHLBI NIH HHS; HL66299/HL/NHLBI NIH HHS; P01 HL066299-09/HL/NHLBI NIH HHS; P01 HL066299-090001/HL/NHLBI NIH HHS; P01 HL066299-099001/HL/NHLBI NIH HHS; P01 HL066299-09S1/HL/NHLBI NIH HHS; R01 HL060024-12/HL/NHLBI NIH HHS; R37 HL060024-14/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Phosphodiesterase Inhibitors; 61413-54-5/Rolipram; 67526-95-8/Thapsigargin
Comments/Corrections
Comment In:
Crit Care Med. 2010 Jun;38(6):1494-6   [PMID:  20502145 ]

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