Hypoxaemia is present in many critically ill patients, and may contribute to encephalopathy. Changes in the passage of large neutral amino acids (LNAAs) across the blood-brain barrier (BBB) with an increased cerebral influx of aromatic amino acids into the brain may concurrently be present and also contribute to encephalopathy, but it has not been established whether hypoxaemia per se may trigger such changes. We measured cerebral blood flow (CBF) in 11 healthy men using the Kety-Schmidt technique and obtained paired arterial and jugular-venous blood samples for the determination of LNAAs by high performance liquid chromatography at baseline and after 9 hours of poikilocapnic normobaric hypoxia (12% O₂). Transcerebral net exchange was determined by the Fick principle, and transport of LNAAs across the BBB was determined mathematically. Hypoxia increased both the systemic and corresponding cerebral delivery of the aromatic amino acid phenylalanine, and the branched-chain amino acids leucine and isoleucine. Despite this, the transcerebral net exchange values and mathematically derived brain extracellular concentrations for all LNAAs were unaffected. In conclusion, the observed changes in circulating LNAAs triggered by hypoxaemia do not affect the transcerebral exchange kinetics of LNAAs to such an extent that their brain extracellular concentrations are affected.

低氧血症存在于许多危重患者中，可能导致脑病。大中性氨基酸（LNAAs）穿过血脑屏障（BBB）的通道变化以及芳香族氨基酸向大脑的脑内流入量增加可能同时存在，也可能导致脑病，但尚未确定低氧血症本身可能触发这种变化。我们使用Kety-Schmidt技术测量了11名健康男性的脑血流量（CBF），并通过高效液相色谱法在基线和脓毒症患者正常低压缺氧9小时后，通过动脉和颈静脉血配对血样测定LNAA（12 ％O ₂）。经Fick原理确定大脑净交换，并通过数学方法确定LNAA在BBB中的转运。低氧增加了芳香族氨基酸苯丙氨酸以及支链氨基酸亮氨酸和异亮氨酸的全身和相应的脑部递送。尽管如此，所有LNAA的经脑净交换值和数学得出的脑细胞外浓度均不受影响。总之，由低氧血症引发的循环LNAA的观察到的变化不会影响LNAA的经脑交换动力学，其程度不会影响它们的脑细胞外浓度。