Bochicchio M, Latronico N, Zani D G, Mariotti M, Morandini L, Acquarolo A M, Candiani A
Institute of Anesthesiology and Intensive Care Medicine, University of Brescia, Italy.
Intensive Care Med. 1990;16(7):444-7. doi: 10.1007/BF01711223.
Ten severely head injured patients (GCS less than or equal to 8), aged 17-62 years, were studied in order to investigate the role of lipoperoxidation in secondary brain damage. No patients had intracranial mass lesions, shock, hypoxemia, fever or sepsis. Blood samples were taken from the jugular bulb and from the right atrium, and thiobarbituric acid reacting substances (TBARS) were measured in plasma by spectrophotometry. Arterio-jugular venous oxygen differences (AVDO2) were obtained in seven patients, in order to estimate cerebral blood flow. Jugular TBARS (TBARSj) were always elevated (from To, to 2 h after injury) and correlated in a linear fashion with TBARS of right atrium (TBARSv): r = 0.74, p less than 0.001. TBARSj and AVDO2 are closely correlated, in accordance with an exponential function (R = 0.45, p less than 0.001) which describes how any cerebral perfusion derangement determines high levels of TBARSj, confirming lipoperoxidation as a key factor in the final common pathway of secondary posttraumatic brain damage.
为了研究脂质过氧化在继发性脑损伤中的作用,对10例年龄在17 - 62岁、严重颅脑损伤(格拉斯哥昏迷评分小于或等于8分)的患者进行了研究。所有患者均无颅内占位性病变、休克、低氧血症、发热或败血症。从颈静脉球和右心房采集血样,采用分光光度法测定血浆中的硫代巴比妥酸反应物质(TBARS)。为了评估脑血流量,对7例患者进行了动脉 - 颈静脉血氧差(AVDO2)测定。颈静脉TBARS(TBARSj)总是升高的(从受伤后即刻到2小时),并且与右心房的TBARS(TBARSv)呈线性相关:r = 0.74,p < 0.001。TBARSj与AVDO2密切相关,符合指数函数(R = 0.45,p < 0.001),该函数描述了任何脑灌注紊乱如何导致TBARSj水平升高,证实脂质过氧化是创伤后继发性脑损伤最终共同途径中的关键因素。