The mechanism of cellular dysfunction after ischemia and reperfusion

缺血再灌注后细胞功能障碍的机制

• 批准号: 61480328
• 负责人: OGAWA Ryo
• 金额: $ 2.24万
• 依托单位: Nippon Medical School (1987)Gunma University (1986)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (B)
• 财政年份: 1986
• 资助国家: 日本
• 起止时间: 1986 至 1987
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-61480328/
• 关键词: Ischemia and reperfusion; cellular injury; lipoperoxide; ショック.スーパーオキシドデイスムターゼ; 酸素遊離基; ショック; 細胞障害; スーパーオキシドデイスムターゼ; 虚血; 再循環; 活性酸素; 化学発光; キサンチン酸化酵素; スーパーオキシドディスムターゼ; 脳虚血; 内臓虚血

the present study was undertaken to clarify the mechanism and to develop the preventive measures of cellular dysfunction induced by ischemia and reperfusion. The results are summarized as followed:(1)The rats with cardiac arrest for 7 min showed an incresed lipoperoxide (LPO) in the brain and disturbed ambulation frequency. Nicardipine and nimodipine given prior to the cardiac arrest showed a protective effect on the CNS against anoxia.(2)The rats with various types of shock such as hemorrhagic shock, endotoxin shock and splanchnic ischemia shock depicted significant elevations of hepatic LPO concentration, concomittantly with marked increases in Xanthine oxidase (XOD) and significant decreases in Superoxide dismutase (SOD).(3)The cellular dysfunction was certified in a model in which the lung was placed in an oxygen free radical production system.(4)The production of oxygen free radicals in the cells was detected by a bioluminescence machine using a lusiferine as a photo-intensifier applied on a tissue homogenates.(5)The effectiveness of various measures to prevent lipoperoxidation were evaluated in rats with endotoxin shock or splanchnic ischemia shock. A high dose of SOD elevated the survival rate significantly.

本研究旨在阐明缺血和再灌注引起的细胞功能障碍的机制并制定预防措施。结果如下： (1)心脏骤停7 min的大鼠脑内过氧化脂(LPO)升高，行走频率紊乱。心脏骤停前给予尼卡地平和尼莫地平对中枢神经系统缺氧具有保护作用。(2)失血性休克、内毒素休克、内脏缺血性休克等多种休克大鼠肝脏LPO浓度显着升高，并伴有黄嘌呤氧化酶（XOD）显着增加，超氧化物歧化酶（SOD）显着降低。（3）细胞功能障碍在将肺置于氧自由基产生系统中的模型。(4)使用荧光素作为应用于组织匀浆的光增强剂，通过生物发光机检测细胞中氧自由基的产生。(5)在患有内毒素休克或内脏缺血休克的大鼠中评估了各种预防脂质过氧化的措施的有效性。高剂量的SOD显着提高了存活率。

项目成果

Ogawa R.;Bitoh H.;Ohi Y.: J. Anesthesia. 2. 36-42 (1988)

Okawa R.；Bitoh H.；Ohi Y.：J. 麻醉。

Kunimoto.F;Morita T;Ogawa R: Circulatory Shock. 21. 15-22 (1987)

Kunimoto.F；Morita T；Okawa R：循环性休克。

Ogawa,R.: "The role of oxygen free radicals in the pathogenesis of cellular injury in the shock." J. Nippon Medical School. 55. 36-42 (1988)

Okawa,R.：“氧自由基在休克细胞损伤发病机制中的作用。”

小川龍: 日本歯科大学雑誌. 55. 4-12 (1988)

小川龙：日本齿科大学杂志 55. 4-12 (1988)。

Kunimoto,F.Morita,T.Ogawa,R.Fujita,T.: "Inhibition of lipid peroxidation improves survival rate of endotoxemic rats" Circulatory Shock. 21. 15-22 (1987)

Kunimoto，F.Morita，T.Okawa，R.Fujita，T.：“抑制脂质过氧化可提高内毒素血症大鼠的存活率”循环休克。