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首页> 外文期刊>American Journal of Physiology >L-NIL prevents renal microvascular hypoxia and increase of renal oxygen consumption after ischemia-reperfusion in rats
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L-NIL prevents renal microvascular hypoxia and increase of renal oxygen consumption after ischemia-reperfusion in rats

机译：L-NIL可防止肾微血管缺氧和大鼠缺血再灌注后肾脏氧消耗的增加

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Even though renal hypoxia is believed to play a pivotal role in the development of acute kidney injury, no study has specifically addressed the alterations in renal oxygenation in the early onset of renal ischemia-reperfusion (I/R). Renal oxygenation depends on a balance between oxygen supply and consumption, with the nitric oxide (NO) as a major regulator of microvascular oxygen supply and oxygen consumption. The aim of this study was to investigate whether I/R induces inducible NO synthase (iNOS)-dependent early changes in renal oxygenation and the potential benefit of iNOS inhibitors on such alterations. Anesthetized Sprague-Dawley rats underwent a 30-min suprarenal aortic clamping with or without either the nonselective NO synthase inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) or the selective iNOS inhibitor L-N6-(1-iminoethyl)lysine hydrochloride (L-NIL). Cortical (CμPO2) and outer medullary (MμPO2) microvascular oxygen pressure (μPO2), renal oxygen delivery (DO2ren), renal oxygen consumption (V?O2ren), and renal oxygen extraction (O2ER) were measured by oxygen-dependent quenching phosphorescence techniques throughout 2 h of reperfusion. During reperfusion renal arterial resistance and oxygen shunting increased, whereas renal blood flow, CμPO 2, and MμPO2 (-70, -42, and -42%, respectively, P 0.05), V?O2ren, and DO2ren (-70%, P 0.0001, and -28%, P 0.05) dropped. Whereas L-NAME further decreased DO2ren, V?O2ren, CμPO2, and MμPO2 and deteriorated renal function, L-NIL partially prevented the drop of DO 2ren and μPO2, increased O2ER, restored V?O2ren and metabolic efficiency, and prevented deterioration of renal function. Our results demonstrate that renal I/R induces early iNOS-dependent microvascular hypoxia in disrupting the balance between microvascular oxygen supply and V?O2ren, whereas endothelial NO synthase activity is compulsory for the maintenance of this balance. L-NIL can prevent ischemic-induced renal microvascular hypoxia. Copyright ? 2009 the American Physiological Society.
机译：尽管据信肾缺氧在急性肾损伤的发展中发挥关键作用，但没有具体研究肾缺血再灌注（I / R）早期发病中肾氧化的改变。肾氧化取决于氧气供应和消耗之间的平衡，用一氧化氮（NO）作为微血管氧供应和氧气消耗的主要调节剂。本研究的目的是研究I / R是否诱导诱导型没有合酶（INOS）依赖性早期变化肾氧合和INOS抑制剂对这种改变的潜在益处。麻醉的Sprague-Dawley大鼠接受了30分钟的超级主动脉夹层，没有非选择性没有合成酶抑制剂Nω-Nitro-L-精氨酸甲酯（L-Name）或选择性InOS抑制剂L-N6-（1-亚氨基乙基）赖氨酸盐酸盐（L-NIL）。皮质（CμPO2）和外髓内（MμPO2）微血管氧压（μPO2），肾氧递送（DO2REN），通过氧依赖性猝灭磷光技术通过氧依赖性猝灭磷光技术测量肾氧耗制性（V≤0℃）和肾氧萃取（o2er） 2小时再灌注。在再灌注肾动脉抵抗和氧气旋转期间，肾血流，CμPO2和MμPO2（分别为P <0.05），V≤0，和DO2REN（-70％）（-70％）（-70％）（-70％）（-70％）（-70％）（-70％ ，P＆ 0.0001，-28％，p <0.05）掉落。虽然L-name进一步减少了DO2REN，V？OEN，CμPO2和MμPO2和肾功能劣化，L-NIL部分地阻止了DO 2RN和μPO2，增加O2er，恢复了V？OEN和代谢效率，并阻止肾脏劣化功能。我们的结果表明，肾I / R在中断微血管氧气供应和vα之间的平衡时诱导早期的依赖性微血管缺氧，而内皮没有合成酶活性用于维持这种平衡。 L-Nil可以防止缺血诱导的肾微血管缺氧。版权？ 2009年美国生理社会。

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