Chonghaile Martina Ni, Higgins Brendan D, Costello Joseph, Laffey John G
Department of Anaesthesia, Clinical Sciences Institute, and the Lung Biology Group, National Centre for Biomedical Engineering Sciences, National University of Ireland, Galway, Ireland.
Anesthesiology. 2008 Nov;109(5):837-48. doi: 10.1097/ALN.0b013e3181895fb7.
Hypercapnic acidosis protects against lung injury after ischemia-reperfusion, endotoxin-induced and ventilation-induced lung injury. The effects of hypercapnic acidosis in the setting of established pulmonary sepsis are not known. The authors investigated whether hypercapnic acidosis -- induced by adding carbon dioxide to inspired gas -- would be beneficial or deleterious in established Escherichia coli pneumonia in an in vivo model, in the presence and absence of antibiotic therapy.
Adult male Sprague-Dawley rats were anesthetized and ventilated. In the first set of experiments, rats were anesthetized, E. coli (5-6.4 x 10(9)/ml colony-forming units) was instilled intratracheally, and the animals were allowed to recover. After 6 h, during which time a severe pneumonia developed, they were reanesthetized and randomly assigned to normocapnia (fraction of inspired carbon dioxide [Fico(2)] = 0.00, n = 10) or hypercapnic acidosis (Fico(2) = 0.05, n = 10). The second set of experiments was performed in a manner identical to that of series 1, but all rats (n = 10 per group) were given intravenous ceftriaxone (30 mg/kg) at randomization. All animals received normocapnia or hypercapnic acidosis for 6 h, and the severity of lung injury was assessed.
In the absence of antibiotic therapy, hypercapnic acidosis reduced the pneumonia-induced increase in peak airway pressure and the decrease in static lung compliance compared with control conditions. In the presence of antibiotic therapy, which substantially reduced lung bacterial counts, hypercapnic acidosis significantly attenuated the extent of pneumonia-induced histologic injury.
Hypercapnic acidosis reduced the magnitude of the lung injury induced by established E. coli pneumonia.
高碳酸血症性酸中毒可预防缺血-再灌注、内毒素诱导及通气诱导的肺损伤后的肺损伤。高碳酸血症性酸中毒在已确诊的肺部脓毒症中的作用尚不清楚。作者研究了在体内模型中，在使用和不使用抗生素治疗的情况下，通过向吸入气体中添加二氧化碳诱导的高碳酸血症性酸中毒对已确诊的大肠杆菌肺炎是有益还是有害。
成年雄性Sprague-Dawley大鼠麻醉后进行通气。在第一组实验中，大鼠麻醉后经气管内注入大肠杆菌（5-6.4×10⁹/ml菌落形成单位），然后让动物恢复。6小时后，此时已发生严重肺炎，再次麻醉并将动物随机分为正常碳酸血症组（吸入二氧化碳分数[FiCO₂]=0.00，n=10）或高碳酸血症性酸中毒组（FiCO₂=0.05，n=10）。第二组实验的进行方式与第一组相同，但所有大鼠（每组n=10）在随机分组时均给予静脉注射头孢曲松（30mg/kg）。所有动物接受正常碳酸血症或高碳酸血症性酸中毒6小时，评估肺损伤的严重程度。
在未使用抗生素治疗的情况下，与对照条件相比，高碳酸血症性酸中毒降低了肺炎诱导的气道峰压升高和静态肺顺应性降低。在使用抗生素治疗的情况下，这显著降低了肺部细菌计数，高碳酸血症性酸中毒显著减轻了肺炎诱导的组织学损伤程度。
高碳酸血症性酸中毒减轻了已确诊的大肠杆菌肺炎所致肺损伤的程度。
