Liposome-encapsulated hemoglobin does not exacerbate endotoxin-induced lung injury

Reuven Rabinovici, Andreas Spirig, Fizan Abdullah, Daniel Roger Phillip, Philip Ovadia, Alan Rudolph

Research output: Contribution to journalArticle

Abstract

Objective: To test the hypothesis that liposome encapsulated hemoglobin (LEH), an experimental oxygen-carrying fluid, exacerbates endotoxin-induced lung injury in the rat. Design: Prospective, randomized animal study. Setting: University animal laboratory. Methods: Anesthetized Sprague-Dawley rats (n = 8-13) were infused with LEH (10% of estimated total blood volume) or vehicle (0.9% NaCl). Thirty minutes later, Escherichia coli endotoxin (3.6 mg/kg, iv) or vehicle (0.9% NaCl) was administered, and skeletal muscle oxygen tension as well as lung injury were assessed at 2, 4, and 8 hrs. Oxygen tension was measured using a miniaturized thin film oxygen sensor placed in the rectus abdominis muscle, and lung injury was evaluated by determining lung weights, lung myeloperoxidase activity, lung tissue tumor necrosis factor-alpha level, and protein concentration in bronchoalveolar lavage fluid. Results: The intravenous bolus injection of E. coli endotoxin elevated lung water content (33% ± 5%; p <.01 vs. sham controls), myeloperoxidase activity (56% ± 6%; p <.01), and tumor necrosis factor- alpha production (1320 ± 154 pg/g lung tissue; p <.05 vs. undetected levels in sham controls), as well as induced protein accumulation in bronchoalveolar lavage fluid (258% ± 38%; p <.01) and skeletal muscle hypoxia (52 ± 8 mm Hg; p <.05). Pretreatment with LEH, which when infused alone did not induce lung injury, had no effect on these responses. Conclusion: In this specific model of endotoxin-induced lung injury, LEH does not exacerbate microvascular leakage and leukosequestration, the hallmarks of adult respiratory distress syndrome.

Original languageEnglish (US)
Pages (from-to)1924-1930
Number of pages7
JournalCritical Care Medicine
Volume28
Issue number6
StatePublished - 2000
Externally publishedYes

Fingerprint

Lung Injury
Endotoxins
Liposomes
Hemoglobins
Lung
Oxygen
Bronchoalveolar Lavage Fluid
Peroxidase
Skeletal Muscle
Tumor Necrosis Factor-alpha
Rectus Abdominis
Muscle Tonus
Adult Respiratory Distress Syndrome
Laboratory Animals
Blood Volume
Intravenous Injections
Sprague Dawley Rats
Proteins
Weights and Measures
Muscles

Keywords

  • Adult respiratory distress syndrome
  • Blood substitutes
  • Cytokines

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Rabinovici, R., Spirig, A., Abdullah, F., Phillip, D. R., Ovadia, P., & Rudolph, A. (2000). Liposome-encapsulated hemoglobin does not exacerbate endotoxin-induced lung injury. Critical Care Medicine, 28(6), 1924-1930.

Liposome-encapsulated hemoglobin does not exacerbate endotoxin-induced lung injury. / Rabinovici, Reuven; Spirig, Andreas; Abdullah, Fizan; Phillip, Daniel Roger; Ovadia, Philip; Rudolph, Alan.

In: Critical Care Medicine, Vol. 28, No. 6, 2000, p. 1924-1930.

Research output: Contribution to journalArticle

Rabinovici, R, Spirig, A, Abdullah, F, Phillip, DR, Ovadia, P & Rudolph, A 2000, 'Liposome-encapsulated hemoglobin does not exacerbate endotoxin-induced lung injury', Critical Care Medicine, vol. 28, no. 6, pp. 1924-1930.
Rabinovici R, Spirig A, Abdullah F, Phillip DR, Ovadia P, Rudolph A. Liposome-encapsulated hemoglobin does not exacerbate endotoxin-induced lung injury. Critical Care Medicine. 2000;28(6):1924-1930.
Rabinovici, Reuven ; Spirig, Andreas ; Abdullah, Fizan ; Phillip, Daniel Roger ; Ovadia, Philip ; Rudolph, Alan. / Liposome-encapsulated hemoglobin does not exacerbate endotoxin-induced lung injury. In: Critical Care Medicine. 2000 ; Vol. 28, No. 6. pp. 1924-1930.
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AB - Objective: To test the hypothesis that liposome encapsulated hemoglobin (LEH), an experimental oxygen-carrying fluid, exacerbates endotoxin-induced lung injury in the rat. Design: Prospective, randomized animal study. Setting: University animal laboratory. Methods: Anesthetized Sprague-Dawley rats (n = 8-13) were infused with LEH (10% of estimated total blood volume) or vehicle (0.9% NaCl). Thirty minutes later, Escherichia coli endotoxin (3.6 mg/kg, iv) or vehicle (0.9% NaCl) was administered, and skeletal muscle oxygen tension as well as lung injury were assessed at 2, 4, and 8 hrs. Oxygen tension was measured using a miniaturized thin film oxygen sensor placed in the rectus abdominis muscle, and lung injury was evaluated by determining lung weights, lung myeloperoxidase activity, lung tissue tumor necrosis factor-alpha level, and protein concentration in bronchoalveolar lavage fluid. Results: The intravenous bolus injection of E. coli endotoxin elevated lung water content (33% ± 5%; p <.01 vs. sham controls), myeloperoxidase activity (56% ± 6%; p <.01), and tumor necrosis factor- alpha production (1320 ± 154 pg/g lung tissue; p <.05 vs. undetected levels in sham controls), as well as induced protein accumulation in bronchoalveolar lavage fluid (258% ± 38%; p <.01) and skeletal muscle hypoxia (52 ± 8 mm Hg; p <.05). Pretreatment with LEH, which when infused alone did not induce lung injury, had no effect on these responses. Conclusion: In this specific model of endotoxin-induced lung injury, LEH does not exacerbate microvascular leakage and leukosequestration, the hallmarks of adult respiratory distress syndrome.

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