Pathophysiologie des Akuten Lungenversagens bei Schwerbrandverletzten mit Inhalationstrauma

Translated title of the contribution: Pathophysiology of acute lung injury in severe burn and smoke inhalation injury

M. O. Maybauer, S. Rehberg, D. L. Traber, David Herndon, D. M. Maybauer

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

This review article describes the pathophysiological aspects of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), induced by combined burn and smoke inhalation and examines various therapeutic approaches. The injury results in a fall in arterial oxygenation as a result of airway obstruction, increased pulmonary transvascular fluid flux and loss of hypoxic pulmonary vasoconstriction. The changes in cardiopulmonary function are mediated by reactive oxygen and nitrogen species. Nitric oxide (NO) is generated by both inducible and constitutive isoforms of nitric oxide synthase (NOS). Recently, neuronal NOS emerged as a major component within the pathogenesis of ARDS. NO rapidly combines with the oxygen radical superoxide to form reactive and highly toxic nitrogen species such as peroxynitrite. The control of NO formation involves poly(ADP-ribose) polymerase and its ability to up-regulate the activity of nuclear transcription factors through ribosylation. In addition, present data support a major role of the bronchial circulation in the injury, as blockage of bronchial blood flow will also minimize the pulmonary injury. Current data suggest that cytotoxins and activated cells are formed in the airway and carried to the parenchyma.

Original languageGerman
Pages (from-to)805-812
Number of pages8
JournalAnaesthesist
Volume58
Issue number8
DOIs
StatePublished - Aug 2009

Fingerprint

Smoke Inhalation Injury
Acute Lung Injury
Nitric Oxide
Adult Respiratory Distress Syndrome
Reactive Oxygen Species
Inhalation Burns
Reactive Nitrogen Species
Lung
Nitric Oxide Synthase Type I
Peroxynitrous Acid
Poly(ADP-ribose) Polymerases
Poisons
Cytotoxins
Wounds and Injuries
Lung Injury
Airway Obstruction
Vasoconstriction
Nitric Oxide Synthase
Smoke
Superoxides

Keywords

  • Acute respiratory distress syndrome
  • Airway
  • Nitric oxide
  • Peroxynitrite
  • Recombinant human activated protein C

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Maybauer, M. O., Rehberg, S., Traber, D. L., Herndon, D., & Maybauer, D. M. (2009). Pathophysiologie des Akuten Lungenversagens bei Schwerbrandverletzten mit Inhalationstrauma. Anaesthesist, 58(8), 805-812. https://doi.org/10.1007/s00101-009-1560-x

Pathophysiologie des Akuten Lungenversagens bei Schwerbrandverletzten mit Inhalationstrauma. / Maybauer, M. O.; Rehberg, S.; Traber, D. L.; Herndon, David; Maybauer, D. M.

In: Anaesthesist, Vol. 58, No. 8, 08.2009, p. 805-812.

Research output: Contribution to journalArticle

Maybauer, MO, Rehberg, S, Traber, DL, Herndon, D & Maybauer, DM 2009, 'Pathophysiologie des Akuten Lungenversagens bei Schwerbrandverletzten mit Inhalationstrauma', Anaesthesist, vol. 58, no. 8, pp. 805-812. https://doi.org/10.1007/s00101-009-1560-x
Maybauer, M. O. ; Rehberg, S. ; Traber, D. L. ; Herndon, David ; Maybauer, D. M. / Pathophysiologie des Akuten Lungenversagens bei Schwerbrandverletzten mit Inhalationstrauma. In: Anaesthesist. 2009 ; Vol. 58, No. 8. pp. 805-812.
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