The effect of N-acetylcysteine on oxygen transport and uptake in patients with fulminant hepatic failure
The effect of N-acetylcysteine on oxygen transport and uptake in patients with fulminant hepatic failure
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DOI：
10.1002/hep.510270520
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发表时间：
1998-05-01
期刊：
影响因子：
13.5
通讯作者：
Lee, A
中科院分区：
文献类型：
--
作者：
Walsh, TS;Hopton, P;Lee, A
我们研究了N-乙酰半胱氨酸对暴发性肝功能衰竭患者血液动力学变量、氧输送（Do（2））、氧消耗（Vo（2））和氧提取的影响，使用独立的方法测定Do（2）和Vo（2），从而消除了数学耦合的影响，这可能会使以前的研究产生偏差。在11例严重暴发性肝功能衰竭患者中，我们记录了N-乙酰半胱氨酸在标准输注方案的前5小时内的血流动力学效应，并同时使用基于呼吸气体分析的方法测量Vo（2）。我们将生理变化与血浆N-乙酰半胱氨酸浓度相关，并将该组与7例接受安慰剂输注的患者进行比较。观察到对N-乙酰半胱氨酸的可变血流动力学反应，与安慰剂组相比无显著差异，且与血浆药物浓度无关。在任何患者中观察到的Do（2）和Vo（2）之间最显著的关系预测，当Do（2）增加100 mL. min（-1）.m（-2）时，Vo（2）增加13 mL. min（-1）.m（-2）;在8例患者中，Vo（2）在观察范围内与Do（2）无关。在接受N-乙酰半胱氨酸的组中，输注1小时后，Vo（2）较基线有小幅增加（平均6 [SD 6] mL.min（-1）.m（-2））（P <0.01），但与安慰剂组相比，变化无显著差异，且不持续。在研究期间，N-乙酰半胱氨酸输注并没有增加氧提取或导致全血乳酸水平或碱过剩的改善。我们得出结论，N-乙酰半胱氨酸输注并没有导致严重暴发性肝衰竭患者的总体Vo（2）或组织缺氧的临床标志物的临床相关改善。
We have investigated the effect of N-acetylcysteine on hemodynamic variables, oxygen delivery (Do(2)), oxygen consumption (Vo(2)), and oxygen extraction in patients with fulminant hepatic failure using independent methods of determining Do(2) and Vo(2), thereby eliminating the effect of mathematical coupling, which may have biased previous studies. in 11 patients with severe fulminant hepatic failure, we documented the hemodynamic effects of N-acetylcysteine during the first 5 hours of a standard infusion regime and simultaneously measured Vo(2) using a method based on respiratory gas analysis. We related physiological changes to plasma N-acetylcysteine concentrations, and compared this group with 7 patients who received placebo infusions. A variable hemodynamic response to N-acetylcysteine was observed that did not differ significantly in comparison with the placebo group, and did not correlate with plasma drug concentrations. The most significant relationship observed between Do(2) and Vo(2) in any patient predicted a 13-mL.min(-1).m(-2) increase in Vo(2) when Do(2) increased by 100 mL.min(-1).m(-2); in 8 patients, Vo(2) was independent of Do(2) over the range observed. Tn the group that received N-acetylcysteine, a small (mean 6 [SD 6] mL.min(-1).m(-2)) increase in Vo(2) occurred in comparison with baseline after 1 hour of infusion (P < .01), but changes were not significantly different from the placebo group and were not sustained. N-Acetylcysteine infusion did not increase oxygen extraction or result in an improvement in whole-blood lactate levels or base excess during the study period, We conclude that N-acetylcysteine infusion does not result in clinically relevant improvements in global Vo(2), or in clinical markers of tissue hypoxia in patients with severe fulminant hepatic failure.