The role of renal sympathetic nervous system in the pathogenesis of ischemic acute renal failure
The role of renal sympathetic nervous system in the pathogenesis of ischemic acute renal failure
复制标题
DOI：
10.1016/j.ejphar.2003.09.036
复制
发表时间：
2003-11-28
影响因子：
5
通讯作者：
Matsumura, Y
中科院分区：
文献类型：
--
作者：
Fujii, T;Kurata, H;Matsumura, Y
我们研究了肾交感神经系统在缺血/再灌注诱导的大鼠急性肾功能衰竭进展中的作用。在对侧肾切除后2周，通过夹闭左肾动、静脉45 min再灌注诱导急性肾功能衰竭。肾静脉血浆去甲肾上腺素浓度在再灌注后立即显著升高，此后下降，但仍高于再灌注后24 h。肾缺血时肾交感神经活动明显增强。肾去神经支配或给予神经节阻滞剂喷妥宁（5 mg/ kg i. v.）缺血前5 min给药可减轻缺血/再灌注引起的肾功能损害及肾小管蛋白管型和肾小管坏死等组织学损害。再灌注后肾静脉去甲肾上腺素水平的升高被肾去神经支配或喷托溴铵治疗抑制。因此，肾交感神经的手术或药物阻断防止缺血/再灌注诱导的急性肾衰竭的进展，从而表明肾交感神经系统在缺血性急性肾衰竭的发展中起重要作用。(C)2003 Elsevier B. V.保留所有权利。
We investigated the role of renal sympathetic nervous system in the progression of ischemia/reperfusion-induced acute renal failure in rats. Acute renal failure was induced by clamping the left renal artery and vein for 45 min followed by reperfusion, 2 weeks after the contralateral nephrectomy. Renal venous plasma norepinephrine concentrations markedly and significantly increased immediately after reperfusion, thereafter, the increased level declined but remained higher even at 24 h after reperfusion. Renal sympathetic nerve activity was significantly augmented during the renal ischemia. Renal denervation or the administration of pentolinium, a ganglion blocking agent, (5 mg/ kg i.v.) at 5 min before ischemia attenuated the ischemia/reperfusion-induced renal dysfunction and histological damage, such as proteinaceous casts in tubuli and tubular necrosis. The elevation of renal venous norepinephrine levels after reperfusion was suppressed by renal denervation or pentolinium treatment. Thus, a surgical or pharmacological blockade of renal sympathetic nerve prevents the progression of ischemia/reperfusion-induced acute renal failure, thereby suggesting that renal sympathetic nervous system plays an important role in the development of the ischemic acute renal failure. (C) 2003 Elsevier B.V. All rights reserved.