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在没有肾神经的情况下,心房利钠肽没有预防内毒素诱导的急性肾衰竭的潜力。

Atrial natriuretic peptide has no potential to protect against endotoxin-induced acute renal failure in the absence of renal nerves.

作者信息

Hiki N, Mimura Y

机构信息

Third Department of Surgery, The University of Tokyo, Japan.

出版信息

Endocr J. 1998 Feb;45(1):75-81. doi: 10.1507/endocrj.45.75.

DOI:10.1507/endocrj.45.75
PMID:9625449
Abstract

Atrial natriuretic peptide (ANP) has been shown to have the potential to restore renal function after ischemic injury, an underlying component of endotoxin (Et)-induced acute renal failure, and is known to counteract renal sympathetic nerve activity in renal function. We have recently found that renal denervation restores the Et-induced renal dysfunction. The purpose of this study was to examine effects of ANP infusion on the Et-induced acute renal failure in the absence of renal nerves. Ten to 14 days after bilateral renal denervation (DNX), Wistar rats (250 to 300 g body wt) were used in the acute experiment. Rats with intact renal nerves (INN) served as controls. Following control clearance measurements, rats were intravenously injected with 4 mg/kg Et (Escherichia coli, 055: B5). During endotoxemia, rats were infused with 10 microg/kg/h ANP or saline vehicle. Et injection reduced the glomerular filtration rate (GFR) significantly in saline-infused INN and DNX rats. ANP infusion restored the greatly reduced GFR to the pre-endotoxemia level in DNX rats but not in INN rats. There was significant difference between the ANP- and saline-infused DNX rats in the percentage change relative to the basal GFR value during the ANP infusion period. ANP infusion did not improve the hyponatriuresis and oliguria after Et administration, which is independent of renal nerves. In conclusion, ANP infusion has a minor reno-protective effect in rats with Et-induced acute renal failure in the absence of the renal nerves.

摘要

心房利钠肽(ANP)已被证明有潜力在缺血性损伤后恢复肾功能,缺血性损伤是内毒素(Et)诱导的急性肾衰竭的一个潜在组成部分,并且已知其能抵消肾功能中的肾交感神经活动。我们最近发现肾去神经支配可恢复Et诱导的肾功能障碍。本研究的目的是在无肾神经的情况下,研究ANP输注对Et诱导的急性肾衰竭的影响。双侧肾去神经支配(DNX)后10至14天,将Wistar大鼠(体重250至300克)用于急性实验。具有完整肾神经(INN)的大鼠作为对照。在进行对照清除率测量后,给大鼠静脉注射4mg/kg Et(大肠杆菌,055:B5)。在内毒素血症期间,给大鼠输注10μg/kg/h ANP或生理盐水。Et注射使输注生理盐水的INN和DNX大鼠的肾小球滤过率(GFR)显著降低。ANP输注使DNX大鼠大幅降低的GFR恢复到内毒素血症前水平,但在INN大鼠中未恢复。在ANP输注期间,ANP输注组和生理盐水输注组的DNX大鼠相对于基础GFR值的百分比变化存在显著差异。ANP输注并未改善Et给药后的低钠尿症和少尿症,这与肾神经无关。总之,在无肾神经的情况下,ANP输注对Et诱导的急性肾衰竭大鼠具有轻微的肾保护作用。

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引用本文的文献

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Recent advances in natriuretic peptide research.利钠肽研究的最新进展。
J Cell Mol Med. 2007 Nov-Dec;11(6):1263-71. doi: 10.1111/j.1582-4934.2007.00125.x.