Effects of high-volume plasmapheresis on ammonia, urea, and amino acids in patients with acute liver failure
Effects of high-volume plasmapheresis on ammonia, urea, and amino acids in patients with acute liver failure
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DOI：
10.1111/j.1572-0241.2001.03706.x
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发表时间：
2001-04
影响因子：
9.8
通讯作者：
J. Clemmesen;J. Kondrup;L. Nielsen;F. Larsen;P. Ott
中科院分区：
文献类型：
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作者：
J. Clemmesen;J. Kondrup;L. Nielsen;F. Larsen;P. Ott
目的：急性肝衰竭（ALF）患者尿素生成严重受损，谷氨酰胺合成氨解毒作用起重要保护作用。本研究的目的是检查治疗性高容量血浆置换（HVP）对动脉浓度和内脏氨、尿素和氨基酸（特别是谷氨酰胺）交换速率的影响。方法：对11例发展为III-IV级肝性脑病的ALF患者，在7小时内置换8l血浆。通过肝静脉置管测量氨、尿素和氨基酸的内脏交换率。结果：HVP对氨和谷氨酰胺的去除率分别为1 μmol/min和27 μmol/min。动脉血氨由160±65 μmol/L降至114±50 μmol/L （p < 0.001）。相比之下，动脉谷氨酰胺仅在1791±1655 ~ 1764±1875 μmol/L （NS）范围内发生微小变化。这表明全身谷氨酰胺合成速率提高了27 μmol/min。内脏交换速率（HVP前vs后）如下：氨为- 93±101 μmol/min vs - 70±80 μmol/min (NS)；尿素-氮分别为0.08±1.64和- 0.31±0.45 mmol/min (NS)；丙氨酸分别为- 73±151 μmol/min和12±83 μmol/min (p < 0.05)；谷氨酰胺：132±246 μmol/min vs 186±285 μmol/min (NS)，负值为释放。结论：ALF患者在HVP期间动脉氨氮降低。数据表明，HVP的这种作用可以解释为肝脏尿素合成增加，也可能是肌肉组织中谷氨酰胺合成增加。
OBJECTIVE:In acute liver failure (ALF), urea production is severely impaired, and detoxification of ammonia by glutamine synthesis plays an important protective role. The aim of this study was to examine the effects of therapeutic high-volume plasmapheresis (HVP) on arterial concentrations and splanchnic exchange rates of ammonia, urea, and amino acids—in particular, glutamine.METHODS:A quantity of 8 L of plasma was exchanged over the course of 7 h in 11 patients with ALF after development of hepatic encephalopathy grade III–IV. Splanchnic exchange rates of ammonia, urea, and amino acids were measured by use of liver vein catheterization.RESULTS:HVP removed ammonia and glutamine at a rate of 1 μmol/min and 27 μmol/min, respectively. Arterial ammonia decreased from 160 ± 65 to 114 ± 50 μmol/L (p < 0.001). In contrast, arterial glutamine was only minimally changed from 1791 ± 1655 to 1764 ± 1875 μmol/L (NS). This implied that the rate of systemic glutamine synthesis was increased by 27 μmol/min. Splanchnic exchange rates (before vs after HVP) were as follows: for ammonia, −93 ± 101 versus− 70 ± 80 μmol/min (NS); urea-nitrogen, 0.08 ± 1.64 versus− 0.31 ± 0.45 mmol/min (NS); alanine, −73 ± 151 versus 12 ± 83 μmol/min (p < 0.05); and glutamine: 132 ± 246 versus 186 ± 285 μmol/min (NS), with negative values denoting release.Conclusions:Arterial ammonia decreased during HVP in patients with ALF. The data suggest that this effect of HVP could be explained by increased hepatic urea synthesis and possibly by increased glutamine synthesis in muscle tissue.