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大鼠实验性肝硬化中钠潴留的发生与肝功能的一个临界阈值有关。

The onset of sodium retention in experimental cirrhosis in rats is related to a critical threshold of liver function.

作者信息

Wensing G, Sabra R, Branch R A

机构信息

Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232.

出版信息

Hepatology. 1990 May;11(5):779-86. doi: 10.1002/hep.1840110511.

DOI:10.1002/hep.1840110511
PMID:2347553
Abstract

Although sodium retention is a common complication in advanced liver disease, the relationship between liver and kidney function in cirrhosis has not been well established. The objective of this study was to investigate this relationship in an experimental model of cirrhosis induced in phenobarbital-treated rats by weekly intragastric administration of carbon tetrachloride. Liver function, measured by the aminopyrine breath test, and urinary sodium excretion on a constant salt diet, were measured weekly. Administration of carbon tetrachloride led to cirrhosis, sodium retention, ascites and a reduction in liver function as measured by the amino pyrine breath test in all 15 rats surviving the first 8 wk. The time to develop sodium retention (defined as a decrease in urinary sodium excretion rate to less than 0.3 mmol/24 hr) varied from 9 to 19 wk. The aminopyrine breath test rate constant of elimination was reduced from 24 x 10(-3) min-1 +/- 2 x 10(-3) min-1 at the start of carbon tetrachloride administration by 61% +/- 10% at the time sodium retention occurred. A linear decrease was seen in aminopyrine breath test rate constant of elimination in the weeks preceding the onset of sodium retention. Sodium retention occurred when aminopyrine breath test rate contant of elimination was reduced to a critical threshold of 10 x 10(-3) +/- 1 x 10(-3) min-1, and then permitted to recover above this level by withdrawal of carbon tetrachloride. Sodium retention occurred when the aminopyrine breath test rate constant of elimination fell below the threshold; this was followed by spontaneous diuresis when aminopyrine breath test rate constant of elimination improved above 10 x 10(-3) +/- 1 x 10(-3) min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

尽管钠潴留是晚期肝病的常见并发症,但肝硬化患者肝肾功能之间的关系尚未完全明确。本研究的目的是在苯巴比妥处理的大鼠中,通过每周胃内给予四氯化碳诱导肝硬化的实验模型来研究这种关系。每周测量通过氨基比林呼吸试验测定的肝功能以及在恒定盐饮食下的尿钠排泄。给予四氯化碳导致肝硬化、钠潴留、腹水,并且在最初8周存活的所有15只大鼠中,通过氨基比林呼吸试验测量的肝功能下降。出现钠潴留的时间(定义为尿钠排泄率降至低于0.3 mmol/24小时)为9至19周。在给予四氯化碳开始时,氨基比林呼吸试验消除速率常数为24×10⁻³ min⁻¹±2×10⁻³ min⁻¹,在出现钠潴留时降低了61%±10%。在钠潴留发生前的几周内,氨基比林呼吸试验消除速率常数呈线性下降。当氨基比林呼吸试验消除速率常数降至临界阈值10×10⁻³±1×10⁻³ min⁻¹时出现钠潴留,然后通过停用四氯化碳使其恢复到该水平以上。当氨基比林呼吸试验消除速率常数低于阈值时出现钠潴留;随后当氨基比林呼吸试验消除速率常数提高到10×10⁻³±1×10⁻³ min⁻¹以上时出现自发性利尿。(摘要截短于250字)

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The onset of sodium retention in experimental cirrhosis in rats is related to a critical threshold of liver function.大鼠实验性肝硬化中钠潴留的发生与肝功能的一个临界阈值有关。
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