THE EARLY PHASE OF EXPERIMENTAL ACUTE-RENAL-FAILURE .6. THE INFLUENCE OF FUROSEMIDE
THE EARLY PHASE OF EXPERIMENTAL ACUTE-RENAL-FAILURE .6. THE INFLUENCE OF FUROSEMIDE
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DOI：
10.1007/bf00581260
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发表时间：
1981-01-01
影响因子：
4.5
通讯作者：
SCHNERMANN, J
中科院分区：
文献类型：
--
作者：
MASON, J;KAIN, H;SCHNERMANN, J
研究了呋塞米（给予大鼠）的剂量高到足以引起强烈的利尿作用并抑制肾小管肾小球反馈机制，是否对肾毒素（硝酸铀酰）或局部缺血引起的急性肾衰竭有任何保护作用。Henle袢的微灌注显示肾小管速尿浓度为5 μ g/ml。10-5摩尔数l-1是完全抑制致密斑对NaCl浓度升高的肾小管肾小球反馈反应所必需的。在肾毒素之前或之后全身输注呋塞米以在肾小管中达到这样的浓度导致肾功能的改善，但在缺血之前或之后给药时没有效果。然而，尿中呋塞米浓度的测量结果证实，应用了足够的量来抑制反馈机制。呋塞米仅在具有阻塞性或肾毒性发病机制的急性肾衰竭模型中是有益的，其中它通过冲洗有害物质而不是通过抑制肾小管肾小球反馈机制起作用。
Whether furosemide, given in doses [to rats] high enough to induce a strong diuresis and to inhibit the mechanism of tubuloglomerular feedback, offers any protection from acute renal failure induced by a nephrotoxin [uranyl nitrate] or ischemia was studied. Microperfusion of the loop of Henle revealed that a tubular furosemide concentration of 5 .cntdot. 10-5 mol .cntdot. l-1 was necessary to fully inhibit the tubuloglomerular feedback response to a raised NaCl concentration at the macula densa. The infusion of furosemide systemically to achieve such concentrations in the tubule resulted in an improvement in renal function when given before or after the nephrotoxin but was without effect when given before or after ischemia. Measurements of furosemide concentrations in the urine, however, confirmed that sufficient amounts were applied to inhibit the feedback mechanism. Furosemide is only beneficial in models of acute renal failure with an obstructive or nephrotoxic pathogenesis, in which it acts by flushing out the noxious material and not by inhibiting the mechanism of tubuloglomerular feedback.