Cristol J P, Thiemermann C, Guérin M C, Torreilles J, de Paulet A C
INSERM U58, Montpellier, France.
J Lipid Mediat Cell Signal. 1996 Jan;13(1):9-17. doi: 10.1016/0929-7855(95)00010-0.
To assess the role of superoxide (O2-) and nitric oxide (NO) in ischaemic-reperfusion-induced acute renal failure, we investigated whether an activation of the L-arginine-NO pathway contributes to ischaemia-reperfusion-induced kidney membrane peroxidation by measurement of 4-hydroxynonenal (HNE) content in anaesthetized rats submitted to acute renal ischaemia. Following ischaemia-reperfusion injury, renal blood flow (RBF) was significantly reduced, while renal vascular resistance was significantly increased. Infusion of neither L-arginine nor D-arginine led to a recovery of RBF. L-Arginine, but not D-arginine, caused a significant increase in HNE accumulation in the ischaemic kidney. L-Arginine infusion enhanced the degree of lipid peroxidation afforded by ischaemia-reperfusion injury in the kidney suggesting that products of the endogenous L-arginine-NO pathway may react with O2- to initiate lipid peroxidation.
为评估超氧化物（O2-）和一氧化氮（NO）在缺血再灌注诱导的急性肾衰竭中的作用，我们通过测量接受急性肾缺血的麻醉大鼠的4-羟基壬烯醛（HNE）含量，研究了L-精氨酸-NO途径的激活是否会导致缺血再灌注诱导的肾膜过氧化。缺血再灌注损伤后，肾血流量（RBF）显著降低，而肾血管阻力显著增加。输注L-精氨酸和D-精氨酸均未导致RBF恢复。L-精氨酸而非D-精氨酸导致缺血肾脏中HNE积累显著增加。输注L-精氨酸增强了缺血再灌注损伤在肾脏中引起的脂质过氧化程度，这表明内源性L-精氨酸-NO途径的产物可能与O2-反应引发脂质过氧化。
