Notorious oxide.
Notorious oxide.
复制标题
臭名昭著的氧化物。
DOI：
10.1097/aln.0b013e318259a8e8
复制
发表时间：
2012
期刊：
影响因子：
8.8
通讯作者：
Nagele,Peter
中科院分区：
文献类型：
--
作者：
Nagele,Peter
一氧化二氮有一个不寻常的药理学副作用，与其麻醉作用无关：它使维生素B12失活。维生素B12的失活是不可逆的，并导致同型半胱氨酸在细胞中的随后积累，因为蛋氨酸合酶，一种将同型半胱氨酸转化为蛋氨酸的重要酶，依赖于维生素B12的活性形式，因此也被一氧化二氮失活。同型半胱氨酸的积累可以通过血浆总同型半胱氨酸（结合和未结合同型半胱氨酸）的增加来临床测量，其幅度与一氧化二氮暴露的持续时间和剂量密切相关。一氧化二氮的这种作用早已为人们所知，并在动物和成年人身上反复显示，但直到现在才在幼儿身上发现。连同最近关于青少年的报告1，Pichardo等人在本期《麻醉学》中进行的研究2，提供了有关一氧化二氮对幼儿高半胱氨酸影响的第一个证据，对此作者应该表示祝贺。毫不奇怪，作者发现在他们的32名3-126个月的儿童队列中，氧化亚氮麻醉后血浆总同型半胱氨酸增加了25%。绝对增加很小（+ 1.3 μmol/L），并且显著低于先前报告中的发现（+ 9.4 μmol/L），1但这种差异可能是由于后一项研究中一氧化二氮暴露时间显著延长所致。此外，Pichardo等人在一氧化二氮暴露后24小时仅获得了一次同型半胱氨酸测量结果，这可能错过了血浆同型半胱氨酸峰值，而血浆同型半胱氨酸峰值通常在停止一氧化二氮给药后立即出现。但这一发现的临床意义是什么？血浆同型半胱氨酸急性升高的临床意义是什么？什么是同型半胱氨酸？
Nitrous oxide has an unusual pharmacological side-effect that is unrelated to its anesthetic action: it inactivates vitamin B12. The inactivation of vitamin B12 is irreversible and causes a subsequent accumulation of homocysteine in the cell, because methionine synthase, an important enzyme that converts homocysteine to methionine, depends on the active form of vitamin B12 and is therefore also inactivated by nitrous oxide. The accumulation of homocysteine can be measured clinically by an increase in plasma total homocysteine (bound and unbound homocysteine), the magnitude of which is tightly correlated with the duration and dose of nitrous oxide exposure. This effect of nitrous oxide has long been known and repeatedly shown in animals and adult humans, but not in young children–until now. Together with a recent report in adolescents, 1 the study by Pichardo et al. in this issue of Anesthesiology, 2 provides the first evidence regarding the effects of nitrous oxide on homocysteine in young children, for which the authors should be congratulated. Not surprisingly, the authors found a 25% increase in plasma total homocysteine after nitrous oxide anesthesia in their cohort of 32 children aged 3–126 months. The absolute increase was small (+ 1.3 μmol/L) and substantially lower than found in a previous report (+ 9.4 μmol/L), 1 but this discrepancy may be explained by the substantially longer nitrous oxide exposure times in the latter study. Furthermore, Pichardo et al. obtained only a single homocysteine measurement 24 hours after nitrous oxide exposure, which may have missed the plasma homocysteine peak which typically occurs immediately after the cessation of nitrous oxide administration.The study by Pichardo et al. thus confirms–not unexpectedly–that nitrous oxide causes a dose-dependent increase in plasma homocysteine in children. But what is the clinical relevance of this finding? What is the clinical relevance of an acute increase in plasma homocysteine? What is homocysteine?