TY -的A2 -劳夫,阿布杜尔盟,中川圭佑盟,田中Ryosuke盟——Donouchi Masahide盟——神田,玛莎雅盟——Kamada Saaya盟——Kobuchi血缘AU -塔洼村,Masashi盟——Matsumura AU - Ohkita康夫守PY - 2022 DA - 2022/02/25 TI -胸主动脉的血管内皮功能障碍大鼠缺血性急性肾损伤:硫酸吲哚酚SP - 7547269六世的贡献- 2022 AB -慢性肾脏疾病(CKD)和心血管疾病有关,和硫酸吲哚酚的参与(是),一种尿毒症毒素,有被认为是其中的一个原因。众所周知,是诱发血管功能障碍通过生产过剩的活性氧(ROS)。另一方面,在血管功能障碍的参与与急性肾损伤(AKI)并不完全理解。因此,我们调查这个问题使用的大鼠胸主动脉缺血性阿基。阻塞引起的缺血性阿基是左肾动脉和静脉的45分钟,随后再灌注2周后对侧肾切除术。一天后再灌注,在肾功能显著恶化增加血浆肌酐证明了这一点。此外,血液水平显著增加是由于肾功能恶化。七天,28天之后再灌注、血液与肾功能的改善水平下降。值得注意的是,acetylcholine-induced血管舒张恶化随着时间的推移,再灌注后,这与肾功能的恢复。此外,再灌注后28天,我们观察到维管组织中活性氧产量显著增加。 Next, we administered AST-120, a spherical adsorbent charcoal, after reperfusion to assess whether the vascular endothelial dysfunction associated with the ischemic AKI was due to a temporary increase in blood IS levels. AST-120 reduced the temporary increase in blood IS levels after reperfusion without influencing renal function, but did not restore the impaired vascular reactivity. Thus, in ischemic AKI, we confirmed that the vascular endothelial function of the thoracic aorta is impaired even after the recovery of kidney injury, probably with excessive ROS production. IS, which increases from ischemia to early after reperfusion, may not be a major contributor to the vascular dysfunction associated with ischemic AKI. SN - 1942-0900 UR - https://doi.org/10.1155/2022/7547269 DO - 10.1155/2022/7547269 JF - Oxidative Medicine and Cellular Longevity PB - Hindawi KW - ER -