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; 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.

本研究的目的是阐明该机制并开发缺血和再灌注引起的细胞功能障碍的预防措施。结果总结如下：（1）用心脏骤停7分钟的大鼠在大脑中显示出脂过氧化物（LPO）的递增和干扰的行动频率。心脏骤停之前给出的nicardipine和nimodipine对中枢神经系统具有保护作用。（2）具有各种冲击的大鼠，例如出血性休克，内毒素休克，内毒素休克和斑点缺血性休克，表明肝LPO浓度的显着升高，同一致，在XANTHINE氧化范围内增加了Xodise and xodsice and xodsic and xodise and xodsic and xodsic andsive and supperax （SOD）。（3）在一个模型中认证了细胞功能障碍，其中将肺放置在氧气自由基生产系统中。（4）通过使用lusiferine用作光摄像机将氧化剂施加在植物中的各种程度上（5）有效性（5）的有效性。内毒素休克或隐性缺血冲击。高剂量的SOD显着提高了生存率。