Wakabayashi Y, Kikawada R
Department of Medicine, University of Kitasato Medical School, Sagamihara, Japan.
Am J Physiol. 1996 May;270(5 Pt 2):F784-9. doi: 10.1152/ajprenal.1996.270.5.F784.
Because myoglobin is a potent inhibitor of nitric oxide (NO), we tested whether myoglobin infusion results in renal vasoconstriction and dysfunction, on which L-arginine, a source of NO, has a protective effect in sedated, nondehydrated, and nonacidotic rabbits. The infusion of myoglobin (375 mg/kg) resulted in a decrease in renal blood flow, an increase in renal vascular resistance, and a decrease in creatine clearance associated with a decrease in urinary excretory rate of nitrite/nitrate and guanosine 3',5'-cyclic monophosphate (cGMP). These values 1-2 h after the infusion were significantly different from baseline levels. Co-administration of L-arginine (150 mg/kg bolus followed by 150 mg.kg(-1).min(-1) reversed these changes significantly with attenuation of urinary excretory rate of nitrite/nitrate and cGMP. This study suggests that the myoglobin-induced renal vasoconstriction and dysfunction and protective effect of L-arginine on these outcomes could be mediated through the NO system.
由于肌红蛋白是一氧化氮（NO）的强效抑制剂，我们测试了输注肌红蛋白是否会导致肾血管收缩和功能障碍，而作为NO来源的L-精氨酸对处于镇静、非脱水且非酸中毒状态的兔子具有保护作用。输注肌红蛋白（375mg/kg）导致肾血流量减少、肾血管阻力增加以及肌酐清除率降低，同时伴有亚硝酸盐/硝酸盐和鸟苷3',5'-环磷酸（cGMP）尿排泄率下降。输注后1-2小时这些值与基线水平有显著差异。联合给予L-精氨酸（150mg/kg推注，随后以150mg·kg⁻¹·min⁻¹）可显著逆转这些变化，同时亚硝酸盐/硝酸盐和cGMP的尿排泄率降低。本研究表明，肌红蛋白诱导的肾血管收缩和功能障碍以及L-精氨酸对这些结果的保护作用可能通过NO系统介导。
