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Research ArticleOriginal Contributions

Time Course of Physiologic Variables in Response to Ventilator-Induced Lung Injury

David J Dries, Dana A Simonson, Alexander B Adams and John J Marini
Respiratory Care January 2007, 52 (1) 31-37;
David J Dries
Pulmonary Research Laboratory, Regions Hospital, St Paul, Minnesota.
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Dana A Simonson
Pulmonary Research Laboratory, Regions Hospital, St Paul, Minnesota.
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Alexander B Adams
Pulmonary Research Laboratory, Regions Hospital, St Paul, Minnesota.
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  • For correspondence: [email protected]
John J Marini
Pulmonary Research Laboratory, Regions Hospital, St Paul, Minnesota.
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Abstract

BACKGROUND: The time course of the physiological derangements that result from ventilatorinduced lung injury has not been adequately described. Similarly, the regional topographies of pleural pressure and tissue edema have not been carefully mapped for this injury process.

METHODS: Lung injury was induced in 9 normal pigs by ventilating for 6 hours at a transpulmonary pressure of 35 cm H2O, with the animals in the supine position. Eight additional normal pigs received right thoracotomy to place pleural-surface-pressure sensors prior to an identical period and intensity of injurious ventilation. Gas exchange and lung mechanics were tracked in all the animals. Cytokines (tumor necrosis factor alpha, interleukin 6, and interleukin 8) in peripheral blood were assayed at 2 hour intervals, beginning at the onset of mechanical ventilation, from all the animals.

RESULTS: After a brief “induction” period, PaO2 and tidal volume declined steadily in the animals that were ventilated to induce lung injury. The rate of decline was greater in the animals that received thoracotomy. The pleural pressure gradient steadily increased from ventral to dorsal. The serum cytokine levels did not evolve with developing injury, but cytokines were elevated at the onset of ventilation. Tissue edema, as assessed by the ratio of wet weight to dry weight, was greater in the thoracotomized animals than in the nonthoracotomized animals, and tissue edema tended to be greater in the caudal lung regions than in the cephalad lung regions.

CONCLUSIONS: Following the induction period, the development of ventilator-induced lung injury progressed steadily and then plateaued, as assessed by quantitative physiology variables during 6 hours of ventilation at a transpulmonary pressure of 35 cm H2O. Greater injury developed in animals that had a coexisting potential insult (thoracotomy). Injury development was not paralleled by bloodborne inflammatory cytokines.

  • ventilator-induced lung injury
  • thoracotomy
  • acute respiratory failure
  • mechanical ventilation
  • animal studies

Footnotes

  • Correspondence: E-mail: alex.b.adams{at}healthpartners.com.
  • Alexander B Adams MPH RRT FAARC presented a version of this paper at the 49th OPEN FORUM of the International Respiratory Congress, American Association for Respiratory Care, held December 8–11, 2003, in Las Vegas, Nevada.

  • Copyright © 2007 by Daedalus Enterprises Inc.
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Respiratory Care: 52 (1)
Respiratory Care
Vol. 52, Issue 1
1 Jan 2007
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Time Course of Physiologic Variables in Response to Ventilator-Induced Lung Injury
David J Dries, Dana A Simonson, Alexander B Adams, John J Marini
Respiratory Care Jan 2007, 52 (1) 31-37;

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Time Course of Physiologic Variables in Response to Ventilator-Induced Lung Injury
David J Dries, Dana A Simonson, Alexander B Adams, John J Marini
Respiratory Care Jan 2007, 52 (1) 31-37;
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Keywords

  • ventilator-induced lung injury
  • thoracotomy
  • acute respiratory failure
  • mechanical ventilation
  • animal studies

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