Document Detail

Heliox attenuates lung inflammation and structural alterations in acute lung injury.
MedLine Citation:
PMID:  16193495     Owner:  NLM     Status:  MEDLINE    
Low-density gas mixtures, such as heliox, were shown to reduce the work of breathing and facilitate the distribution of inspired gas. Since supplemental ventilatory and oxygen requirements may lead to pulmonary inflammation and structural alterations, we hypothesized that by reducing these requirements, heliox breathing may attenuate the acute inflammatory and structural changes associated with acute lung injury. Spontaneously breathing neonatal pigs were anesthetized, instrumented, supported with continuous positive airway pressure (CPAP), injured with oleic acid, and randomized to nitrox (n = 6) or heliox (n = 5).F(I)O(2) was titrated for pulse oximetry (SpO(2)) 95 +/- 2% for 4 hr. Gas exchange and pulmonary mechanics were measured. Lungs were analyzed for myeloperoxidase (MPO), interleukin-8 (IL-8), and histomorphometery. Relationships between physiologic indices and cumulative lung structure and inflammatory indices were evaluated. With heliox, compliance was significantly greater, while tidal volume, frequency, minute ventilation, F(I)O(2), arterial carbon dioxide tension (PaCO(2)), MPO, and IL-8 were significantly lower compared to nitrox. The expansion index and number of exchange units were significantly greater with heliox, while the exchange unit area (EUA) was smaller. MPO was significantly and positively correlated with F(I)O(2) (r = 0.76) and EUA (r = 0.63), and negatively correlated with number of open exchange units/field (r = -0.73). Compared to breathing nitrox, these data indicate that heliox improved the distribution of inspired gas, thereby recruiting more gas exchange units, improving gas exchange efficiency, reducing ventilatory and oxygen requirements, and attenuating lung inflammation. These data suggest that heliox breathing may have the combined therapeutic benefits of attenuating lung inflammation by reducing mechanical and oxidative stress in the clinical management of acute lung injury.
Ursula S Nawab; Suzanne M Touch; Tami Irwin-Sherman; Thomas J Blackson; Jay S Greenspan; Guangfa Zhu; Thomas H Shaffer; Marla R Wolfson
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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:  Pediatric pulmonology     Volume:  40     ISSN:  8755-6863     ISO Abbreviation:  Pediatr. Pulmonol.     Publication Date:  2005 Dec 
Date Detail:
Created Date:  2005-11-01     Completed Date:  2006-03-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8510590     Medline TA:  Pediatr Pulmonol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  524-32     Citation Subset:  IM    
Copyright Information:
(c) 2005 Wiley-Liss, Inc.
Division of Neonatology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, USA.
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MeSH Terms
Animals, Newborn
Continuous Positive Airway Pressure
Disease Models, Animal
Helium / pharmacology*
Interleukin-8 / metabolism
Lung / metabolism,  pathology*
Nitrogen / pharmacology
Oxygen / blood,  pharmacology*
Peroxidase / metabolism
Pneumonia / chemically induced,  drug therapy*,  pathology
Respiratory Function Tests
Respiratory Mechanics
Grant Support
1P20 RR20173-01/RR/NCRR NIH HHS
Reg. No./Substance:
0/Interleukin-8; 37291-87-5/nitrox; 58933-55-4/heliox; 7440-59-7/Helium; 7727-37-9/Nitrogen; 7782-44-7/Oxygen; EC

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