Schrier R W, Cronin R E, Miller P, de Torrenté A, Burke T, Bulger R
Yale J Biol Med. 1978 May-Jun;51(3):355-9.
Infusion of 0.75 μ g/kgbw/min norepinephrine (NE), for 40 minutes, into one renal artery in anesthetized dogs, induced acute renal failure (ARF). Subsequently there was nearly complete reversal of function within 8 weeks. Isotonic saline volume expansion, or renal vasodilation plus diuresis by acetylcholine (into renal artery: 20 μg/min) did not protect against this type of ARF. Volume expansion with either 5 or 20 percent mannitol partly prevented the fall of GFR 3 hours after NE, this protection being correlated with the magnitude of the osmolar clearance at the time of the insult. IV furosemide (10 mg/kg + 10 mg/kg/h; fluid losses replaced) afforded an even better protection. Proximal tubular necrosis in the "protected" kidneys was as severe as in non-protected kidneys. Glomerular cell morphology (scanning electron microscopy) was not altered by the 40-minute NE infusions. Functional "protection" appeared to depend on solute diuresis at the time of insult.
在麻醉犬的一侧肾动脉中以0.75μg/kg体重/分钟的速度输注去甲肾上腺素（NE）40分钟，可诱发急性肾衰竭（ARF）。随后在8周内功能几乎完全恢复。等渗盐水扩容，或通过乙酰胆碱（肾动脉内：20μg/分钟）进行肾血管舒张加利尿，均不能预防此类ARF。用5%或20%的甘露醇扩容可部分预防NE注射3小时后肾小球滤过率（GFR）的下降，这种保护作用与损伤时渗透清除率的大小相关。静脉注射呋塞米（10mg/kg + 10mg/kg/小时；补充液体丢失量）提供了更好的保护。“受保护”肾脏的近端肾小管坏死与未受保护的肾脏一样严重。40分钟的NE输注未改变肾小球细胞形态（扫描电子显微镜观察）。功能性“保护”似乎取决于损伤时的溶质利尿作用。
