Risby T H, Maley W, Scott R P, Bulkley G B, Kazui M, Sehnert S S, Schwarz K B, Potter J, Mezey E, Klein A S
Department of Environmental Health Sciences, Johns Hopkins Medical Institutions, Baltimore, Md.
Surgery. 1994 Jan;115(1):94-101.
Generation of toxic oxygen metabolites at reperfusion may contribute to the injury sustained as a consequence of harvest and ischemic preservation of organ allografts. Because there is a paucity of evidence that this mechanism is operative in human beings, we measured the generation of ethane into the exhaled breath as a biomarker of free radical-mediated lipid peroxidation in human liver transplantation.
A novel technique that increased the previous standard of sensitivity 100-fold was used to measure picomole quantities of ethane in exhaled breath of eight recipients undergoing human orthotopic liver transplantation.
Ethane production correlated closely with the specific events of liver transplantation including the initial reperfusion of the allografts. In every case a twofold to threefold increase in ethane production was superimposed on a stable baseline immediately after reestablishment of portal vein blood flow through the donor liver.
Ethane production was interpreted as evidence of hepatic lipid peroxidation, presumably mediated by toxic metabolites of oxygen occurring at reperfusion. This noninvasive approach allowed localization of the time point at which lipid peroxidation occurred and may facilitate quantification of lipid peroxidation mediated by free radicals and other toxic oxygen metabolites during operation.
再灌注时有毒氧代谢产物的生成可能导致器官同种异体移植物在获取和缺血保存过程中受到损伤。由于缺乏证据表明该机制在人类中起作用，我们测量了呼出气体中乙烷的生成，作为人类肝移植中自由基介导的脂质过氧化的生物标志物。
一种将先前标准灵敏度提高100倍的新技术被用于测量8例接受原位肝移植的受者呼出气体中皮摩尔量的乙烷。
乙烷生成与肝移植的特定事件密切相关，包括同种异体移植物的初始再灌注。在每例病例中，通过供体肝脏重新建立门静脉血流后，乙烷生成立即在稳定的基线水平上增加了两倍至三倍。
乙烷生成被解释为肝脂质过氧化的证据，推测是由再灌注时产生的氧有毒代谢产物介导的。这种非侵入性方法可以确定脂质过氧化发生的时间点，并可能有助于量化手术过程中自由基和其他有毒氧代谢产物介导的脂质过氧化。
