Analysis of intracellular mechanisms and related factors regarding spinal protection by remote preoonditioning

远程预适应脊柱保护的细胞内机制及相关因素分析

基本信息

批准号：
18591697
负责人：
IIDA Hiroki
金额：
$ 2.27万
依托单位：
Gifu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18591697/
关键词：
Aortic clamp and unclamp Spinal ischemia Remote preconditioning Angiotensin II Rho-kinase Free radical Spinal cord tissue oxygen pressure Limb ischemia プレコンディショニング脳血管

项目摘要

Pentobarbital anesthetized rabbits were prepared for measurement of cerebral pial vessel diameter in a cranial window preparation or spinal cord partial tissue oxygen pressure (PtO2). We investigated the experiments according to following protocols.1) We studied the effect of aortic clamping and declamping as a remote preconditioning intervention on cerebral pial vessel diameter. Although infrarenal aortic cross-clamping did not affect pial vessel diameter, release of a 20-min aortic cross-clamp caused pial arterioles to dilate and then constrict. A significant constriction persisted for at least 60 min. To clarify the mechanism of remote preconditioning regarding humoral factor, we examined whether angiotensin II typel receptor blocker, Rho-kinase inhibitor, or free radical scavenger, would affect the respose observed after aortic cross-clamping and release on cerebral vessels. All three drugs significantly attenuated the constriction of pial arterioles. Thus angiotensin II, Rho-kinase, and free radical could be possible to be candidates for humoral factors related to remote conditioning on spinal protection.2) We measured directly the tissue oxygen partial pressure of the spinal cord to assess the efficacy of remote preconditioning in preventing apinal cord ischemic injury in an experimental model. PtO2 were significantly lower in the preconditioning intervention group at 20 min after aortic cross-clamping and 0, 2 min after aortic unclamping. Remote preconditioning performed in fore and hind legs protected the decrease of PtO2 compared with control group. Thus, the effect on PtO2 by such intervention may relate to the mechanism of spinal protection induced by remote preconditioning by transient upper and lower limbs ischemia.

制备戊巴比妥大麻醉兔子，用于测量颅窗制剂中的脑血管直径或脊髓部分组织氧气（PTO2）。我们根据以下方案研究了实验。1）我们研究了主动脉夹紧并逐渐降低作为远程预处理干预对脑血管直径的影响。尽管肾上腺主动脉夹板不影响毛皮血管直径，但释放20分钟的主动脉跨夹具会导致pial小动脉扩张然后收缩。一个显着的收缩持续至少60分钟。为了阐明有关体液因子的远程预处理的机制，我们检查了血管紧张素II打字受体阻滞剂，Rho-激酶抑制剂或自由基清除剂是否会影响主动脉交叉夹紧并在大脑容器上释放后观察到的响应。所有三种药物都大大衰减了伴侣小动脉的收缩。因此，血管紧张素II，Rho-激酶和自由基可以成为与脊柱保护方面的远程调节有关的体液因子的候选。2）我们直接测量了脊髓的组织氧氧部分压力，以评估远程预处理在实验模型中防止Apinal缺血性损伤的远程预处理的功效。主动脉互夹后20分钟，在主动脉解开后20分钟，PTO2在预处理干预组中显着降低。与对照组相比，在前后进行的远程预处理保护PTO2的减少。因此，通过这种干预措施对PTO2的影响可能与瞬态上肢和下肢缺血引起的脊柱保护机制有关。