杨万超：High pressure ventilator-induced lung injury is attenuated by hypercapnic acidosis

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发布日期：2012-08-30 16:35 文章来源：丁香园
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关键词： hypercapnic acidosis ventilation-induced lung injury nuclear factor kappa B cytokines 　 点击次数：

Background:Prophylactic hypercapnic acidosis protects against lung injury duringtherapeutic mechanical ventilation in acute respiratory disorders^1-2. However, the optimal ranges of PaCO₂ and the protection mechanism are not very clear. So, we conducted this study to investigate the influence of moderate and severe hypercapnia on ventilator-induced lung injury induced (VILI) by high pressure ventilation and further study the role of nuclear factor-kB (NF-kB) in the process.

Methods：Rats were ventilated for 4 h, receivingFiCO₂to achieve normocapnia (PaCO₂ at 35-45 mmHg) or moderate (PaCO₂ at 80-100 mmHg) or severe (PaCO₂ at 130-150 mmHg) hypercapnic acidosis. Lung injury was induced by a pressure-controlled ventilatory mode set at a peak inspiratory pressure (PIP) of 30cmH₂O, a positive end-expiratory pressure (PEEP) of 2 cmH₂O, and a frequency of30breaths/min. The hemodynamics and gas exchange, inflammatory parameters (tumor necrosis factor-α, interleukin-1β, and macrophage inflammatory protein-2)were measured, in addition to lung MPO, ICAM-1 expression were analyzed, the activity of NF-kB was evaluated accordingly, as well as pulmonary type II alveolar epithelial cells(AECIIs)apoptosis, neutrophil CD18 and respiratory burst activation, were determinedby flow cytometry.

Results:Compared with eucapnia, both moderate and severe hypercapnic acidosis reversed aggravation in arterial blood pressure and PaO₂/FiO₂, decreased the severity of lung injury, down-regulated the inflammatory cytokines, Lung neutrophil infiltration (MPO), ICAM-1 expression and NF-kB activity (Figure 1) were decreased by hypercapnic acidosis. In addition, hypercapnic acidosis inhibited AECIIs apoptosisand neutrophil respiratory burst and CD18 expression. Based on oxygenation and histologic indices of lung injury, moderate hypercapnic acidosis demonstrated a better protective effect compared with severe hypercapnic acidosis.

Conclusions:Hypercapnic acidosis attenuatedhigh pressure ventilation-induced lung inflammatoryinjury, which may be through the marked attenuation of NF-kBactivityand reduction of oxidative stress from neutrophil-mediated injury, with the optimal range of PaCO₂ maintained at 80-100 mmHg.

Keywords:hypercapnic acidosis; ventilation-induced lung injury; nuclear factor kappa B; cytokines

References

1. The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal

volumes as compared with traditional tidal volumes for acute lung injury and

the acute respiratory distress syndrome. N Eng J Med 2000, 342:1301-1308.

2. Amato MB, Barbas CS, Medeiros DM, Magaldi RB, Schettino GP, Lorenzi- Fihlo

G, Kairalla RA, Deheinzelin D, Munoz C, Oliveira R, Takagaki TY, Carvalho CR:

Effect of a protective-ventilation strategy on mortality in the acute respiratory

distress syndrome. N Eng J Med 1998, 338:347-354.

编辑: lil 作者:丁香园通讯员

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