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老年大鼠肾脏中前列腺素合成改变及钠潴留受损。

Altered prostaglandin synthesis and impaired sodium conservation in the kidneys of old rats.

作者信息

Rathaus M, Greenfeld Z, Podjarny E, Brezis M, Green J, Bernheim J

机构信息

Department of Nephrology, Meir Hospital, Kfar Saba, Israel.

出版信息

Clin Sci (Lond). 1992 Sep;83(3):301-6. doi: 10.1042/cs0830301.

Abstract
  1. The aim of this investigation was to study the role of prostaglandins in the impaired Na+ conservation of the ageing kidney. 2. We measured the urinary excretion of thromboxane B2, 6-keto-prostaglandin F1 alpha and prostaglandin E2 in young (3-4 months) and old (20-21 months) rats after 12, 24 and 36 h of Na+ deprivation. In a separate protocol, we measured prostanoid synthesis by isolated glomeruli, cortical homogenates, medullary slices and papillary slices from young and old rats in basal conditions and after 15 days of dietary Na+ deprivation. 3. In the acute study, urinary excretion of 6-keto-prostaglandin F1 alpha and prostaglandin E2 decreased in young but not in old rats. Urinary excretion of prostaglandin E2 was lower in old rats, but did not vary significantly with Na+ deprivation. 4. In old rats, thromboxane B2 synthesis was increased in all the portions of the kidney except the medulla. Production of 6-keto-prostaglandin F1 alpha was elevated in glomeruli and tended to increase in the cortex. Prostaglandin E2 synthesis was also elevated in the cortex. Thromboxane B2 synthesis tended to increase in the medulla and was enhanced in the papilla. After Na+ deprivation, only glomerular prostaglandin E2 synthesis increased in young rats. In old rats, cortical and papillary synthesis of 6-keto-prostaglandin F1 alpha increased, whereas prostaglandin E2 synthesis did not change. 5. The results suggest increased thromboxane synthesis in the ageing kidney. Increased prostacyclin and prostaglandin E2 synthesis may be an attempt to counteract enhanced thromboxane production.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 本研究的目的是探讨前列腺素在老年肾脏钠潴留受损中的作用。2. 我们测量了年轻(3 - 4个月)和老年(20 - 21个月)大鼠在钠缺乏12、24和36小时后血栓素B2、6 - 酮 - 前列腺素F1α和前列腺素E2的尿排泄量。在另一个实验方案中,我们测量了年轻和老年大鼠在基础状态下以及饮食钠缺乏15天后,分离的肾小球、皮质匀浆、髓质切片和乳头切片中前列腺素的合成。3. 在急性研究中,年轻大鼠6 - 酮 - 前列腺素F1α和前列腺素E2的尿排泄量下降,而老年大鼠则没有。老年大鼠前列腺素E2的尿排泄量较低,但随钠缺乏无显著变化。4. 在老年大鼠中,除髓质外,肾脏各部分血栓素B2的合成均增加。肾小球中6 - 酮 - 前列腺素F1α的产生增加,皮质中也有增加趋势。皮质中前列腺素E2的合成也增加。髓质中血栓素B2的合成有增加趋势,乳头中则增强。钠缺乏后,年轻大鼠仅肾小球前列腺素E2的合成增加。老年大鼠中,皮质和乳头中6 - 酮 - 前列腺素F1α的合成增加,而前列腺素E2的合成无变化。5. 结果表明老年肾脏中血栓素合成增加。前列环素和前列腺素E2合成增加可能是为了对抗血栓素产生的增加。(摘要截短至250字)

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