Document Detail

Hyperventilation induces release of cytokines from perfused mouse lung.
MedLine Citation:
PMID:  9445308     Owner:  NLM     Status:  MEDLINE    
Artificial mechanical ventilation represents a major cause of iatrogenic lung damage in intensive care. It is largely unknown which mediators, if any, contribute to the onset of such complications. We investigated whether stress caused by artificial mechanical ventilation leads to induction, synthesis, and release of cytokines or eicosanoids from lung tissue. We used the isolated perfused and ventilated mouse lung where frequent perfusate sampling allows determination of mediator release into the perfusate. Hyperventilation was executed with either negative (NPV) or positive pressure ventilation (PPV) at a transpulmonary pressure that was increased 2.5-fold above normal. Both modes of hyperventilation resulted in an approximately 1.75-fold increased expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) mRNA, but not of cyclooxygenase-2 mRNA. After switching to hyperventilation, prostacyclin release into the perfusate increased almost instantaneously from 19 +/- 17 pg/min to 230 +/- 160 pg/min (PPV) or 115 +/- 87 pg/min (NPV). The enhancement in TNFalpha and IL-6 production developed more slowly. In control lungs after 150 min of perfusion and ventilation, TNFalpha and IL-6 production was 23 +/- 20 pg/min and 330 +/- 210 pg/min, respectively. In lungs hyperventilated for 150 min, TNFalpha and IL-6 production were increased to 287 +/- 180 pg/min and more than 1,000 pg/min, respectively. We conclude that artificial ventilation might cause pulmonary and systemic adverse reactions by inducing the release of mediators into the circulation.
A N von Bethmann; F Brasch; R Nüsing; K Vogt; H D Volk; K M Müller; A Wendel; S Uhlig
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  157     ISSN:  1073-449X     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  1998 Jan 
Date Detail:
Created Date:  1998-02-05     Completed Date:  1998-02-05     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  263-72     Citation Subset:  AIM; IM    
Biochemical Pharmacology, University of Konstanz, Germany.
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MeSH Terms
Disease Models, Animal*
Epoprostenol / analysis,  secretion*
Interleukin-6 / analysis,  secretion*
Mice, Inbred BALB C
Positive-Pressure Respiration / adverse effects*,  methods
Respiratory Distress Syndrome, Adult / etiology,  immunology*
Time Factors
Tumor Necrosis Factor-alpha / analysis,  secretion*
Ventilators, Negative-Pressure / adverse effects*
Reg. No./Substance:
0/Interleukin-6; 0/Tumor Necrosis Factor-alpha; 35121-78-9/Epoprostenol

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

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