Basic analysis for the mechanisms of septic encephalopathy

为探讨脓毒性脑病（SE）的发病机制，我们着重研究了线粒体功能障碍。第1年，脑肿胀实验表明，与对照组相比，由于Ca ~（2+）负荷，脑肿胀明显（对照组vs 1，6，12，24 h，p<0.05）。第二年，钙保留能力。脓毒症对大肠癌的抑制作用随恢复时间的延长而增加（对照组vs 1、6、12、24 h，p<0.05）。去年，我们研究了线粒体呼吸控制率（RCR）由于Klark电极测定。根据恢复时间，RCR强烈降低。CLP组在恢复后12、24 h的RCR较对照组明显降低（P<0.05），脓毒性脑病时线粒体功能受到抑制。

To investigate the mechanisms of septic Encephalopathy(SE), we focused on the mitochon drial dysfunction. Firts year, The swelling assay suggested that brain has showed significant swelling due to Ca2 + loading comapred to control(control vs 1,6,12,24h, p<0.05). Seccond year, Calcium Retention Capacity. Sepsis significantly inhibited the CRC according to the recovery time(control vs 1,6,12,24h, p<0.05). Last year, we have investigated the mitochondrial respiratory control ratio(RCR) due to Klark elctrode assay. RCR was strongly reduced according to the recovery time. Especially, 12 and 24h after recovery, CLP group showed significant reduction of RCR compare to control(P<0.05).Septic encephalopathy showed the inhibition of mitochondrial function.