Myrianthefs Pavlos M, Briva Arturo, Lecuona Emilia, Dumasius Vidas, Rutschman David H, Ridge Karen M, Baltopoulos George J, Sznajder Jacob Iasha
Division of Pulmonary and Critical Care Medicine, 240 East Huron, McGaw 2-2300, Northwestern University, Chicago, IL 60611, USA.
Am J Respir Crit Care Med. 2005 Jun 1;171(11):1267-71. doi: 10.1164/rccm.200408-998OC. Epub 2005 Mar 11.
Acid-base disturbances, such as metabolic or respiratory alkalosis, are relatively common in critically ill patients. We examined the effects of alkalosis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in the isolated and continuously perfused rat lung model. We found that alveolar fluid reabsorption after 1 hour was impaired by low levels of CO2 partial pressure (PCO2; 10 and 20 mm Hg) independent of pH levels (7.7 or 7.4). In addition, PCO2 higher than 30 mm Hg or metabolic alkalosis did not have an effect on this process. The hypocapnia-mediated decrease of alveolar fluid reabsorption was associated with decreased Na,K-ATPase activity and protein abundance at the basolateral membranes of distal airspaces. The effect of low PCO2 on alveolar fluid reabsorption was reversible because clearance normalized after correcting the PCO2 back to normal levels. These data suggest that hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption. Conceivably, correction of hypocapnic alkalosis in critically ill patients may contribute to the normalization of lung ability to clear edema.
酸碱平衡紊乱，如代谢性或呼吸性碱中毒，在重症患者中较为常见。我们在离体连续灌注大鼠肺模型中研究了碱中毒（低碳酸血症或代谢性碱中毒）对肺泡液体重吸收的影响。我们发现，1小时后的肺泡液体重吸收受到低水平二氧化碳分压（PCO2；10和20毫米汞柱）的损害，且与pH值水平（7.7或7.4）无关。此外，高于30毫米汞柱的PCO2或代谢性碱中毒对该过程没有影响。低碳酸血症介导的肺泡液体重吸收减少与远端气腔基底外侧膜上钠钾ATP酶活性和蛋白丰度降低有关。低PCO2对肺泡液体重吸收的影响是可逆的，因为将PCO2校正回正常水平后清除率恢复正常。这些数据表明，低碳酸血症而非代谢性碱中毒会损害肺泡液体重吸收。可以想象，纠正重症患者的低碳酸血症性碱中毒可能有助于肺清除水肿能力的恢复正常。
