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慢性肾衰竭大鼠棕色脂肪中去甲肾上腺素周转率的改变。

Altered norepinephrine turnover in the brown fat of rats with chronic renal failure.

作者信息

Bigazzi R, Kogosov E, Campese V M

机构信息

Department of Medicine, University of Southern California, Los Angeles.

出版信息

J Am Soc Nephrol. 1994 May;4(11):1896-900. doi: 10.1681/ASN.V4111896.

DOI:10.1681/ASN.V4111896
PMID:7919141
Abstract

Disturbances of the sympathetic nervous system (SNS) have been described in chronic renal failure, but their role in the metabolic derangements of uremia has not been well established. In these studies, SNS activity has been measured in the ventromedial hypothalamic (VMH) nuclei and in the intercostal brown adipose tissue (IBAT) of Sprague Dawley 5/6 nephrectomized or sham-operated rats. SNS activity was determined by calculating the norepinephrine (NE) turnover rate (in picograms per milligram per hour) 3, 6, and 12 h after the inhibition of NE synthesis with L-methyltyrosine. The endogenous NE concentration was significantly (P < 0.01) higher in the VMH (14,567 +/- 1,130 pg/mg wet wt) and IBAT (17,902 +/- 2,308 pg/mg wet wt) of uremic than control rats (9,600 +/- 1,110 and 5,752 +/- 320 pg/mg wet wt, respectively). The turnover rates of NE in the VMH (582 +/- 146 pg/mg per hour) and in the IBAT (1,432 +/- 179 pg/mg/hr) of uremic rats were significantly faster (P < 0.01) than in control rats (192 +/- 96 and 173 +/- 58 pg/mg per hour, respectively). These studies demonstrate a significant increase in NE turnover in the VMH nuclei and IBAT of uremic rats. It is suggested that increased efferent sympathetic nerve discharge from the VMH to the IBAT may play a role in the pathogenesis of malnutrition in uremia.

摘要

慢性肾衰竭患者存在交感神经系统(SNS)紊乱的情况,但其在尿毒症代谢紊乱中的作用尚未完全明确。在这些研究中,测量了Sprague Dawley 5/6肾切除或假手术大鼠的腹内侧下丘脑(VMH)核和肋间棕色脂肪组织(IBAT)中的SNS活性。通过计算用L-甲基酪氨酸抑制去甲肾上腺素(NE)合成后3、6和12小时的NE周转率(皮克/毫克/小时)来确定SNS活性。尿毒症大鼠VMH(14,567±1,130皮克/毫克湿重)和IBAT(17,902±2,308皮克/毫克湿重)中的内源性NE浓度显著高于对照大鼠(分别为9,600±1,110和5,752±320皮克/毫克湿重,P<0.01)。尿毒症大鼠VMH(582±146皮克/毫克/小时)和IBAT(1,432±179皮克/毫克/小时)中的NE周转率显著快于对照大鼠(分别为192±96和173±58皮克/毫克/小时,P<0.01)。这些研究表明尿毒症大鼠VMH核和IBAT中的NE周转率显著增加。提示从VMH到IBAT的传出交感神经放电增加可能在尿毒症营养不良的发病机制中起作用。

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