ROLE OF RENAL NERVES IN SODIUM RETENTION OF CIRRHOSIS AND CONGESTIVE-HEART-FAILURE
ROLE OF RENAL NERVES IN SODIUM RETENTION OF CIRRHOSIS AND CONGESTIVE-HEART-FAILURE
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DOI：
10.1152/ajpregu.1991.260.2.r298
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发表时间：
1991-02-01
影响因子：
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通讯作者：
SAWIN, LL
中科院分区：
文献类型：
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作者：
DIBONA, GF;SAWIN, LL
为明确肾神经在肝硬化和充血性心力衰竭（CHF）肾钠潴留中的作用，本实验采用胆总管结扎（CBDL）致肝硬化和左冠状动脉结扎致心肌梗死（CHF）大鼠模型。 在诱导CBDL或CHF后两周，使患病和假患病（Sham）大鼠经受双侧肾去神经支配（DNX）或假肾去神经支配（神经支配。INN）。 DNX或INN后5天，在所有大鼠中进行26天代谢平衡研究。 第1-6天和第22-26天的每日膳食钠摄入量平均为2.0-3.0 meq/天，第7-21天平均为0.120 meq/天。 在整个研究期间，CBDL和CHF大鼠（INN或DNX）的累积Na平衡大于Sham/CBDL或CHF大鼠。 在正常饮食Na摄入期结束时的第6天（0-6天），在Sham/CBDL或CHF大鼠中，累积Na平衡不受肾脏去神经支配的影响（INN，2.02 +/- 0.19 meq，n = 10; DNX，2.04 +/- 0.17 meq，n = 11），CBDL大鼠（INN，4.21 +/- 0.39 meq，n = 10; DNX，3.78 +/- 0.37 meq，n = 10）或CHF大鼠（INN，3.74 +/-0.72 meq，n = 9; DNX，3.22 +/- 0.55 meq，n = 10）。 第21天，低钠饮食摄入期结束时（第7-21天），在Sham/CBDL或CHF中，累积Na平衡不受肾脏去神经支配的影响（INN，1.53 +/- 0.23 meq; DNX，1.54 +/- 0.26 meq），但显著降低在CBDL（INN，4.05 +/- 0.38 meq; DNX，2.61 +/- 0.27 meq）和CHF（INN，3.72 +/- 0.72 meq; DNX，1.91 +/- 0.48 meq）中，通过肾去神经支配，P < 0.05。 第26天，正常饮食钠摄入期结束时（第22-26天），这结束了代谢平衡研究，在Sham/CBDL或CHF中，累积Na平衡不受肾脏去神经支配的影响（INN，3.71 +/- 0.29 meq; DNX，3.64 +/- 0.35 meq）在CHF中显著降低（P < 0.05）（6.14 +/- 0.85 meq; DNX，4.67 +/- 0.77 meq）。 它的结论是增加肾钠潴留肝硬化和CHF的特点部分取决于增加传出肾交感神经活动。 这是很容易检测到低，但不是正常的饮食钠摄入量。
To define the role of renal nerves in renal Na retention of cirrhosis and congestive heart failure (CHF), experiments were done in rats with cirrhosis due to common bile duct ligation (CBDL) and CHF due to myocardial infarction from left coronary artery ligation. Two weeks after induction of CBDL or CHF, diseased and sham diseased (Sham) rats were subjected to bilateral renal denervation (DNX) or sham renal denervation (innervated. INN). Five days after DNX or INN, 26-day metabolic balance studies were carried out in all rats. Daily dietary Na intake averaged 2.0-3.0 meq/day on days 1-6 and 22-26 and averaged 0.120 meq/day on days 7-21. Cumulative Na balance was greater in CBDL and CHF rats, INN or DNX, than in Sham/CBDL or CHF rats throughout the study. On day 6 at the end of the normal dietary Na intake period (days 0-6), cumulative Na balance was not affected by renal denervation in Sham/CBDL or CHF rats (INN, 2.02 +/- 0.19 meq, n = 10; DNX, 2.04 +/- 0.17 meq, n = 11), CBDL rats (INN, 4.21 +/- 0.39 meq, n = 10; DNX, 3.78 +/- 0.37 meq, n = 10), or CHF rats (INN, 3.74 +/-0.72 meq, n = 9; DNX, 3.22 +/- 0.55 meq, n = 10). On day 21, at the end of the low dietary Na intake period (days 7-21), cumulative Na balance was not affected by renal denervation in Sham/CBDL or CHF (INN, 1.53 +/- 0.23 meq; DNX, 1.54 +/- 0.26 meq) but was significantly decreased (P < 0.05) by renal denervation in CBDL (INN, 4.05 +/- 0.38 meq; DNX, 2.61 +/- 0.27 meq) and CHF (INN, 3.72 +/- 0.72 meq; DNX, 1.91 +/- 0.48 meq). On day 26 at the end of the normal dietary Na intake period (days 22-26), which concluded the metabolic balance study, cumulative Na balance was not affected by renal denervation in Sham/CBDL or CHF (INN, 3.71 +/- 0.29 meq; DNX, 3.64 +/- 0.35 meq) was significantly decreased (P < 0.05) in CHF (6.14 +/- 0.85 meq; DNX, 4.67 +/- 0.77 meq). It is concluded that the increased renal Na retention characteristic of cirrhosis and CHF depends partly on increased efferent renal sympathetic nerve activity. This is readily detected during low but not normal dietary Na intake.