Schölmerich J, Kremer B, Schmidt K, Setyadharma H, Schoenenberger G A
Acta Biol Med Ger. 1980;39(10):1051-72.
Early and adequate shock treatment combined with improved systemic and local therapy practically eliminated primary death of patients with severe burns. In contrast the late mortality, i.e. the fatal outcome during the "burn disease" has not been significantly improved during the last decade. A burn toxin has been discussed as reason of this burn disease. Such a toxic factor has been isolated from burnt mouse and human skin and from the serum of burnt patients as well. Electron microscopic studies in rats revealed similar and comparable mitochondrial alterations of hepatocytes after either a sublethal controlled burn injury or an i.p. application of an equivalent dose of this cutaneous burn toxin. These alterations were dose-dependent. Studies of the liver metabolism of these rats (i.e. gluconeogenesis, urea synthesis and energy metabolism) suggested an inhibited oxidative phosphorylation. Incubation of enzymatically isolated hepatocytes with toxin demonstrated a direct cytotoxic effect of the burn toxin by scanning electron microscopy. Glycogen synthesis and urea synthesis were significantly reduced, hormonal sensibility was partially abolished. These results suggest a disturbance of the cellular energy metabolism via a cell membrane damage. This could be the reason of the decreased host defence of burned patients which causes the fatal outcome in severe burns. Therefore, elimination of burn toxin should be an important point in burn treatment.
早期充分的休克治疗，结合改进的全身和局部治疗，实际上消除了严重烧伤患者的早期死亡。相比之下，在过去十年中，晚期死亡率，即“烧伤病”期间的致命结局并未得到显著改善。一种烧伤毒素被认为是这种烧伤病的原因。这种有毒因子已从烧伤的小鼠和人类皮肤以及烧伤患者的血清中分离出来。对大鼠的电子显微镜研究表明，在亚致死性可控烧伤或腹腔注射等量这种皮肤烧伤毒素后，肝细胞的线粒体改变相似且具有可比性。这些改变是剂量依赖性的。对这些大鼠肝脏代谢（即糖异生、尿素合成和能量代谢）的研究表明氧化磷酸化受到抑制。用毒素孵育酶分离的肝细胞，通过扫描电子显微镜显示烧伤毒素具有直接细胞毒性作用。糖原合成和尿素合成显著减少，激素敏感性部分丧失。这些结果表明，通过细胞膜损伤干扰了细胞能量代谢。这可能是烧伤患者宿主防御能力下降的原因，导致严重烧伤患者出现致命结局。因此，消除烧伤毒素应是烧伤治疗的一个要点。
