Aspiration-induced lung injury: Role of complement

R. Rabinovici, L. F. Neville, F. Abdullah, D. R. Phillip, J. Vernick, K. L L Fong -, L. Hillegas, G. Feuerstein

Research output: Contribution to journalArticle

Abstract

Objectives: To examine the role of complement in the development of acid aspiration-induced lung injury in the rat. It was postulated that inhibition or depletion of complement attenuates aspiration-induced lung injury. Design: Controlled animal trial. Setting: Animal Laboratory, Jefferson Medical College, Philadelphia, PA. Subjects: Anesthetized rats. Interventions: Aspiration was induced by the intratracheal administration of 0.2 mL of 0.1 N hydrochloric acid (n = 7) and lung injury was evaluated by determining water content, myeloperoxidase activity, protein concentration, and leukocyte count in bronchoalveolar lavage fluid. Muscle PO2 was directly measured using a thin-film chamber oxygen sensor and serum tumor necrosis factor-α was assayed by enzyme-linked immunosorbent assay. The effect of complement inhibition by recombinant human soluble complement receptor type 1 (n = 8) or complement depletion by cobra venom factor (n = 7) on lung injury was evaluated. Measurements and Main Results: Acid aspiration induced pulmonary leukosequestration, edema, and a microvascular permeability defect, along with tissue hypoxia. Pretreatment with soluble complement receptor type 1 (complement inhibition) or cobra venom factor (complement depletion) significantly reduced lung edema (-61 ± 7% ;p <.05), eliminated protein accumulation in bronchoalveolar lavage fluid (p <.01), and improved (p <.05) tissue oxygenation. In contrast, there was no effect of soluble complement receptor type 1 or of cobra venom factor on leukosequestration. Conclusions: Acid aspiration induces lung injury through a complement- dependent mechanism that leads to microvascular permeability defects. Therefore, the possibility that complement inhibitors may have a salutary effect in humans with aspiration-induced lung injury should be investigated.

Original languageEnglish (US)
Pages (from-to)1405-1411
Number of pages7
JournalCritical Care Medicine
Volume23
Issue number8
DOIs
StatePublished - 1995
Externally publishedYes

Fingerprint

Lung Injury
Complement Receptors
Bronchoalveolar Lavage Fluid
Capillary Permeability
Complement Inactivating Agents
Acids
Complement C8
Hydrochloric Acid
Laboratory Animals
Pulmonary Edema
Leukocyte Count
Peroxidase
Edema
Proteins
Tumor Necrosis Factor-alpha
Enzyme-Linked Immunosorbent Assay
Oxygen
Muscles
Lung
Water

Keywords

  • adult respiratory distress syndrome
  • complement factors
  • complement receptor
  • critical illness
  • cytokines
  • leukocytes
  • lung
  • lung injury
  • oxygen
  • pneumonia aspiration
  • pulmonary emergencies

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Rabinovici, R., Neville, L. F., Abdullah, F., Phillip, D. R., Vernick, J., Fong -, K. L. L., ... Feuerstein, G. (1995). Aspiration-induced lung injury: Role of complement. Critical Care Medicine, 23(8), 1405-1411. https://doi.org/10.1097/00003246-199508000-00015

Aspiration-induced lung injury : Role of complement. / Rabinovici, R.; Neville, L. F.; Abdullah, F.; Phillip, D. R.; Vernick, J.; Fong -, K. L L; Hillegas, L.; Feuerstein, G.

In: Critical Care Medicine, Vol. 23, No. 8, 1995, p. 1405-1411.

Research output: Contribution to journalArticle

Rabinovici, R, Neville, LF, Abdullah, F, Phillip, DR, Vernick, J, Fong -, KLL, Hillegas, L & Feuerstein, G 1995, 'Aspiration-induced lung injury: Role of complement', Critical Care Medicine, vol. 23, no. 8, pp. 1405-1411. https://doi.org/10.1097/00003246-199508000-00015
Rabinovici R, Neville LF, Abdullah F, Phillip DR, Vernick J, Fong - KLL et al. Aspiration-induced lung injury: Role of complement. Critical Care Medicine. 1995;23(8):1405-1411. https://doi.org/10.1097/00003246-199508000-00015
Rabinovici, R. ; Neville, L. F. ; Abdullah, F. ; Phillip, D. R. ; Vernick, J. ; Fong -, K. L L ; Hillegas, L. ; Feuerstein, G. / Aspiration-induced lung injury : Role of complement. In: Critical Care Medicine. 1995 ; Vol. 23, No. 8. pp. 1405-1411.
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abstract = "Objectives: To examine the role of complement in the development of acid aspiration-induced lung injury in the rat. It was postulated that inhibition or depletion of complement attenuates aspiration-induced lung injury. Design: Controlled animal trial. Setting: Animal Laboratory, Jefferson Medical College, Philadelphia, PA. Subjects: Anesthetized rats. Interventions: Aspiration was induced by the intratracheal administration of 0.2 mL of 0.1 N hydrochloric acid (n = 7) and lung injury was evaluated by determining water content, myeloperoxidase activity, protein concentration, and leukocyte count in bronchoalveolar lavage fluid. Muscle PO2 was directly measured using a thin-film chamber oxygen sensor and serum tumor necrosis factor-α was assayed by enzyme-linked immunosorbent assay. The effect of complement inhibition by recombinant human soluble complement receptor type 1 (n = 8) or complement depletion by cobra venom factor (n = 7) on lung injury was evaluated. Measurements and Main Results: Acid aspiration induced pulmonary leukosequestration, edema, and a microvascular permeability defect, along with tissue hypoxia. Pretreatment with soluble complement receptor type 1 (complement inhibition) or cobra venom factor (complement depletion) significantly reduced lung edema (-61 ± 7{\%} ;p <.05), eliminated protein accumulation in bronchoalveolar lavage fluid (p <.01), and improved (p <.05) tissue oxygenation. In contrast, there was no effect of soluble complement receptor type 1 or of cobra venom factor on leukosequestration. Conclusions: Acid aspiration induces lung injury through a complement- dependent mechanism that leads to microvascular permeability defects. Therefore, the possibility that complement inhibitors may have a salutary effect in humans with aspiration-induced lung injury should be investigated.",
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KW - pulmonary emergencies

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