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溶质排泄在预防去甲肾上腺素诱导的急性肾衰竭中的作用。

Role of solute excretion in prevention of norepinephrine-induced acute renal failure.

作者信息

Schrier R W, Cronin R E, Miller P, de Torrenté A, Burke T, Bulger R

出版信息

Yale J Biol Med. 1978 May-Jun;51(3):355-9.

Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/2595755/eae62e126030/yjbm00132-0117-a.jpg

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