Abstract | INTRODUCTION: METHODS: Male C57BL/6 mice, weighing 20 to 25 g, were exposed to either high-tidal-volume (30 ml/kg) or low-tidal-volume (6 ml/kg) mechanical ventilation with room air for 1 to 5 hours after 200 IU/kg or 400 IU/kg unfractionated heparin and 4 mg/kg or 8 mg/kg enoxaparin administration. Nonventilated mice served as a control group. Evan blue dye, lung wet- to dry-weight ratio, histopathologic grading of epithelium, myeloperoxidase, and gene expression of PAI-1 were measured. The expression of PAI-1 was studied by immunohistochemistry. RESULTS: High-tidal-volume ventilation induced increased microvascular permeability, neutrophil influx, PAI-1 mRNA expression, production of PAI-1 protein, and positive staining of PAI-1 in epithelium in a dose-dependent manner. Lung injury induced by high-tidal-volume ventilation was attenuated with PAI-1-deficient mice and pharmacologic inhibition of PAI-1 activity by low-dose unfractionated heparin and enoxaparin. CONCLUSIONS:
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Authors | Li-Fu Li, Chung-Chi Huang, Horng-Chyuan Lin, Ying-Huang Tsai, Deborah A Quinn, Shuen-Kuei Liao |
Journal | Critical care (London, England)
(Crit Care)
Vol. 13
Issue 4
Pg. R108
( 2009)
ISSN: 1466-609X [Electronic] England |
PMID | 19580651
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Anticoagulants
- DNA Primers
- Enoxaparin
- Plasminogen Activator Inhibitor 1
- RNA, Messenger
- Heparin
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Topics |
- Animals
- Anticoagulants
(therapeutic use)
- Base Sequence
- Body Water
- DNA Primers
- Enoxaparin
(pharmacology, therapeutic use)
- Heparin
(pharmacology, therapeutic use)
- Immunohistochemistry
- Male
- Mice
- Mice, Inbred C57BL
- Plasminogen Activator Inhibitor 1
(genetics)
- Prospective Studies
- RNA, Messenger
(genetics)
- Respiration, Artificial
(adverse effects, methods)
- Reverse Transcriptase Polymerase Chain Reaction
- Ventilator-Induced Lung Injury
(metabolism, pathology, prevention & control)
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