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.

准备戊巴比妥麻醉的兔子，用于测量颅窗制备中的脑软膜血管直径或脊髓部分组织氧压（PtO2）。我们根据以下方案研究了实验。1）我们研究了主动脉钳夹和松开作为远程预处理干预对脑软膜血管直径的影响。尽管肾下主动脉交叉钳夹不影响软脑膜血管直径，但释放 20 分钟的主动脉交叉钳夹会导致软脑膜小动脉扩张然后收缩。明显的收缩持续至少 60 分钟。为了阐明体液因子远程预处理的机制，我们检查了血管紧张素II型受体阻滞剂、Rho激酶抑制剂或自由基清除剂是否会影响主动脉阻断和释放脑血管后观察到的反应。所有三种药物均显着减弱软脑膜小动脉的收缩。因此，血管紧张素 II、Rho 激酶和自由基可能是与远程调节对脊髓保护相关的体液因子的候选者。2) 我们直接测量脊髓的组织氧分压，以评估远程预处理在脊髓保护中的效果。在实验模型中预防脊髓缺血损伤。主动脉阻断后20分钟和主动脉松开后0、2分钟时，预处理干预组的PtO2显着较低。与对照组相比，前腿和后腿进行的远程预处理保护了 PtO2 的减少。因此，这种干预对PtO2的影响可能与短暂性上肢和下肢缺血远程预处理诱导的脊柱保护机制有关。