Kellum J A, Kramer D J, Lee K, Mankad S, Bellomo R, Pinsky M R
Department of Anesthesiology and Critical Care Medicine, University of Pittsburgh Medical Center, PA 15213, USA.
Chest. 1997 May;111(5):1301-5. doi: 10.1378/chest.111.5.1301.
The pathogenesis of hyperlactatemia during sepsis is poorly understood. We have previously described an increase in lactate concentration across the lung in the dog during early endotoxemia. Accordingly, we sought to determine if the lung releases lactate in humans and what relation this has with lung injury.
We measured lactate concentrations across the lung and lung injury scores (LIS) in two groups of patients. Group 1 consisted of nine patients with acute lung injury (LIS > or = 2.0) and elevated lactate concentrations (> 2.0 mmol/L). Group 2 contained 12 patients with no acute lung injury (LIS scores < or = 1.5), with or without increased lactate concentrations. Simultaneous measurements of plasma lactate and blood gases were obtained from indwelling arterial and pulmonary artery catheters. Measurements of cardiac output were also obtained. Lactate measurements were done using a lactate analyzer (YSI; Yellow Springs, Ohio).
For each patient with acute lung injury and hyperlactatemia, an arterial-venous lactate gradient existed demonstrating release of lactate by the lung. This gradient persisted after correction for changes in hemoconcentration across the lung. The lactate gradient across the lung was 0.4 +/- 0.2 mmol/L for group 1 vs 0.05 +/- 0.1 mmol/L for group 2 (p = 0.001). This corresponded to a mean pulmonary lactate flux of 231.3 +/- 211.3 vs 5.0 +/- 37.2 mmol/h (p = 0.001). The lactate flux and the arterial-venous lactate difference correlated with LIS both for the entire sample and for the subgroup with hyperlactatemia (r = 0.69, p < 0.01). Pulmonary lactate flux was not related to arterial lactate levels (r = 0.25).
In patients with acute lung injury and hyperlactatemia, the lung is a major source of lactate and lactate flux correlates with LIS. This lactate flux could explain some of the hyperlactatemia seen in sepsis.
脓毒症期间高乳酸血症的发病机制尚不清楚。我们之前曾描述过，在犬类早期内毒素血症期间，肺部乳酸浓度会升高。因此，我们试图确定人类肺部是否会释放乳酸，以及这与肺损伤有何关系。
我们测量了两组患者的肺部乳酸浓度和肺损伤评分（LIS）。第1组由9例急性肺损伤（LIS≥2.0）且乳酸浓度升高（>2.0 mmol/L）的患者组成。第2组包含12例无急性肺损伤（LIS评分≤1.5）的患者，无论其乳酸浓度是否升高。通过留置动脉和肺动脉导管同时测量血浆乳酸和血气。还测量了心输出量。使用乳酸分析仪（YSI；俄亥俄州黄泉市）进行乳酸测量。
对于每例急性肺损伤和高乳酸血症患者，均存在动静脉乳酸梯度，表明肺部释放乳酸。在校正肺部血液浓缩变化后，该梯度仍然存在。第1组肺部的乳酸梯度为0.4±0.2 mmol/L，第2组为0.05±0.1 mmol/L（p = 0.001）。这相当于平均肺乳酸通量为231.3±211.3 vs 5.0±37.2 mmol/h（p = 0.001）。乳酸通量和动静脉乳酸差异与整个样本以及高乳酸血症亚组的LIS均相关（r = 0.69，p < 0.01）。肺乳酸通量与动脉乳酸水平无关（r = 0.25）。
在急性肺损伤和高乳酸血症患者中，肺是乳酸的主要来源，且乳酸通量与LIS相关。这种乳酸通量可以解释脓毒症中出现的一些高乳酸血症现象。
