IMPROVEMENT BY ACETYLCYSTEINE OF HEMODYNAMICS AND OXYGEN-TRANSPORT IN FULMINANT HEPATIC-FAILURE
IMPROVEMENT BY ACETYLCYSTEINE OF HEMODYNAMICS AND OXYGEN-TRANSPORT IN FULMINANT HEPATIC-FAILURE
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DOI：
10.1056/nejm199106273242604
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发表时间：
1991-06-27
影响因子：
158.5
通讯作者：
WILLIAMS, R
中科院分区：
文献类型：
--
作者：
HARRISON, PM;WENDON, JA;WILLIAMS, R
背景。在过量服用对乙酰氨基酚后早期给药时，静脉注射乙酰半胱氨酸可通过补充减少的谷胱甘肽储备来预防肝坏死。然而，乙酰半胱氨酸如何改善对乙酰氨基酚所致已确立的肝损伤患者的生存率尚不清楚。本研究旨在确定在这种情况下乙酰半胱氨酸的有益作用是否可能是由于氧输送和消耗的增加。
方法。我们研究了乙酰半胱氨酸对12例对乙酰氨基酚所致暴发性肝衰竭患者和8例其他原因所致急性肝衰竭患者的全身血流动力学和氧转运的影响。乙酰半胱氨酸的给药方式为：在15分钟内将150毫克/千克体重的剂量溶于250毫升5%葡萄糖溶液中，然后在4小时内将50毫克/千克的剂量溶于500毫升5%葡萄糖溶液中；在治疗开始前以及方案实施30分钟后进行测量。
结果。在对乙酰氨基酚所致肝衰竭患者中，乙酰半胱氨酸的输注使平均氧输送从856毫升/分钟/平方米体表面积增加到975毫升/分钟/平方米（P = 0.0036），这是由于心脏指数从5.6升/分钟/平方米增加到6.7升/分钟/平方米（P = 0.0021）。尽管全身血管阻力从1296达因·秒·厘米⁻⁵/平方米降低到1113达因·秒·厘米⁻⁵/平方米（P = 0.027），但平均动脉压从88毫米汞柱上升到95毫米汞柱（P = 0.0054）。氧消耗从127毫升/分钟/平方米增加到184毫升/分钟/平方米（P = 0.0007），同时氧摄取率从16%增加到21%（P = 0.022）。其他原因所致急性肝衰竭患者的效果相似。
结论。乙酰半胱氨酸引起的氧输送和消耗的增加可能是其对对乙酰氨基酚所致暴发性肝衰竭患者生存有益的原因。
Background. When administered early after an overdose of acetaminophen, intravenous acetylcysteine prevents hepatic necrosis by replenishing reduced stores of glutathione. How acetylcysteine improves the survival of patients with established liver damage induced by acetaminophen, however, is unknown. This study was undertaken to determine whether the beneficial effect of acetylcysteine under such circumstances could be due to enhancement of oxygen delivery and consumption.Methods. We studied the effect of acetylcysteine on systemic hemodynamics and oxygen transport in 12 patients with acetaminophen-induced fulminant hepatic failure and 8 patients with acute liver failure from other causes. The acetylcysteine was given in a dose of 150 mg per kilogram of body weight in 250 ml of 5 percent dextrose over a period of 15 minutes and then in a dose of 50 mg per kilogram in 500 ml of 5 percent dextrose over a period of 4 hours; measurements were made before treatment began and after 30 minutes of the regimen.Results. In the patients with acetaminophen-induced liver failure, the infusion of acetylcysteine resulted in an increase in mean oxygen delivery from 856 to 975 ml per minute per square meter of body-surface area (P = 0.0036), due to an increase in the cardiac index from 5.6 to 6.7 liters per minute per square meter (P = 0.0021). Mean arterial pressure rose from 88 to 95 mm Hg (P = 0.0054) despite a decrease in systemic vascular resistance from 1296 to 1113 dyn . sec . cm-5 per square meter (P = 0.027). There was an increase in oxygen consumption from 127 to 184 ml per minute per square meter (P = 0.0007) associated with an increase in the oxygen-extraction ratio from 16 to 21 percent (P = 0.022). The effects in the patients with acute liver failure from other causes were similar.Conclusions. The increase in oxygen delivery and consumption in response to acetylcysteine may account for its beneficial effect on survival in patients with fulminant hepatic failure induced by acetaminophen.