Abstract | OBJECTIVE: DESIGN: Randomized, prospective animal study. SETTING: Research laboratory of university-affiliated hospital. SUBJECTS: Anesthetized, male New Zealand Rabbits. INTERVENTIONS: All animals received the same ventilation strategy (tidal volume, 12 mL/kg; positive end-expiratory pressure, 0 cm H2O; rate, 42 breaths/min) and were randomized to receive FiCO2 of 0.00, 0.05, or 0.12 to produce hypocapnia, normocapnia, and hypercapnia, respectively. MEASUREMENTS AND MAIN RESULTS: Alveolar-arterial oxygen gradient was significantly lower with therapeutic hypercapnia, and peak airway pressure was significantly higher with hypocapnic alkalosis. However, neither static lung compliance nor surfactant chemistry (total surfactant, aggregates, or composition) differed among the groups. CONCLUSIONS: At clinically relevant tidal volume, CO2 modulates key physiologic indices of lung injury, including alveolar-arterial oxygen gradient and airway pressure, indicating a potential role in the pathogenesis of ventilator-associated lung injury. These effects are surfactant independent.
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Authors | John G Laffey, Doreen Engelberts, Michelle Duggan, Ruud Veldhuizen, James F Lewis, Brian P Kavanagh |
Journal | Critical care medicine
(Crit Care Med)
Vol. 31
Issue 11
Pg. 2634-40
(Nov 2003)
ISSN: 0090-3493 [Print] United States |
PMID | 14605535
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
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Topics |
- Animals
- Carbon Dioxide
(adverse effects, therapeutic use)
- Hyperventilation
- Hypocapnia
(complications, physiopathology)
- Male
- Rabbits
- Respiratory Distress Syndrome
(etiology, therapy)
- Tidal Volume
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