Guven Hakan, Amanvermez Ramazan, Malazgirt Zafer, Kaya Ekrem, Doganay Zahide, Celik Cemil, Ozkan Kayhan
Department of Emergency, Ondokuz Mayis University School of Medicine, Samsun, Turkey.
J Trauma. 2002 Jul;53(1):66-72. doi: 10.1097/00005373-200207000-00014.
The purpose of this study was to investigate the effects of temperature on oxidative stress in brain stem tissue induced by hemorrhagic shock. We researched the hemorrhagic oxidative stress at various core temperatures using reduced glutathione (GSH) levels and thiobarbituric acid-reactive substances (TBARS) as markers of lipid peroxidation in brain stem homogenate.
Forty rats were divided into four groups, of which one constituted the nonbleeding normothermia control group. In all of the three study groups, 40% of estimated blood volume was removed while they were being held at normothermia, mild hypothermia (32 degrees C), or moderate hypothermia (28 degrees C). Parameters including mean arterial pressure, rectal temperature, and heart and breathing rates were monitored and recorded during the procedures. After an hour at shock state, tissue samples were removed by craniectomy.
The tissue levels of TBARS increased significantly in normothermic and mild hypothermic hemorrhagic shock groups (10.74 nmol/g and 8.26 nmol/g) as compared with the control group (3.50 nmol/g) (p < 0.001). However, the tissue TBARS level in the moderate hypothermia group was only minimally increased (4.53 nmol/g). GSH showed a slight decrease in normothermic and mild hypothermic bleeding rats, and were unchanged in the moderate hypothermic rats.
Moderate systemic hypothermia (28 degrees C) appears to protect brain stem tissue from oxidative stress during severe hemorrhagic shock in rats, as indicated by insignificant change in tissue TBARS and GSH concentrations. These results suggest antioxidant protective effects of moderate systemic hypothermia in metabolically active brain stem tissue during hemorrhagic shock. Similar effects in humans remain to be studied.
本研究旨在探讨温度对失血性休克诱导的脑干组织氧化应激的影响。我们以还原型谷胱甘肽(GSH)水平和硫代巴比妥酸反应性物质(TBARS)作为脑干匀浆中脂质过氧化的标志物,研究了不同核心温度下的出血性氧化应激。
40只大鼠分为四组,其中一组为非出血正常体温对照组。在三个研究组中,当大鼠处于正常体温、轻度低温(32℃)或中度低温(28℃)时,均去除估计血容量的40%。在操作过程中监测并记录包括平均动脉压、直肠温度以及心率和呼吸频率等参数。休克状态持续1小时后,通过颅骨切除术获取组织样本。
与对照组(3.50 nmol/g)相比,正常体温和轻度低温失血性休克组的组织TBARS水平显著升高(分别为10.74 nmol/g和8.26 nmol/g)(p < 0.001)。然而,中度低温组的组织TBARS水平仅略有升高(4.53 nmol/g)。GSH在正常体温和轻度低温出血大鼠中略有下降,而在中度低温大鼠中无变化。
如组织TBARS和GSH浓度变化不显著所示,中度全身低温(28℃)似乎可保护大鼠在严重失血性休克期间脑干组织免受氧化应激。这些结果表明中度全身低温在失血性休克期间对代谢活跃的脑干组织具有抗氧化保护作用。在人类中的类似作用仍有待研究。