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清醒大鼠输注生理盐水或葡萄糖期间的前列腺素E2排泄、尿流量及乳头渗透压

Prostaglandin E2 excretion, urine flow and papillary osmolality during saline or dextrose infusion in the conscious rat.

作者信息

Lote C J, McVicar A J, Thewles A

出版信息

J Physiol. 1983 Mar;336:39-46. doi: 10.1113/jphysiol.1983.sp014564.

Abstract

Conscious rats received infusions at 5.8 ml./hr of either 0.9% NaCl or 5% dextrose, via a tail vein, for 6 hr. During this infusion period, urine was collected from the animals, and the urine volume, sodium concentration and immunoreactive PGE2 were determined. Urine flow in both groups was stable during the 2-6 hr period of the infusion and was not significantly different between the two groups. Sodium output was also stable over the 2-6 hr infusion period but obviously the output of the saline-infused group was higher than that of the dextrose-infused group. Urinary PGE2 output was not significantly different between the groups in the 2-4 hr period (79.4 +/- 8.6 p-mole/2 hr in the saline-infused group, 82.1 +/- 5.7 p-mole/2 hr in the dextrose-infused group). In the 4-6 hr period, PGE2 output remained at this level (82.0 +/- 7.8 p-mole/2 hr) in the dextrose-infused group, but fell significantly (to 53.7 +/- 5.0 p-mole/2 hr) in the saline-infused group. In separate groups of animals which received saline or dextrose infusions as above, renal papillary osmolality was determined. The osmolality was significantly (P less than 0.001) higher in the saline-infused group. It is concluded that renal PGE2 synthesis is unlikely to be directly involved in sodium homeostasis and that PGE2 synthesis as measured by urinary PGE2 excretion is not controlled by the papillary osmolality.

摘要

清醒大鼠通过尾静脉以5.8毫升/小时的速度输注0.9%氯化钠或5%葡萄糖,持续6小时。在输注期间,收集动物尿液,并测定尿量、钠浓度和免疫反应性前列腺素E2。两组在输注的2 - 6小时内尿流稳定,两组之间无显著差异。钠排出量在2 - 6小时输注期间也稳定,但生理盐水输注组的排出量明显高于葡萄糖输注组。在2 - 4小时期间,两组间尿前列腺素E2排出量无显著差异(生理盐水输注组为79.4±8.6皮摩尔/2小时,葡萄糖输注组为82.1±5.7皮摩尔/2小时)。在4 - 6小时期间,葡萄糖输注组前列腺素E2排出量维持在该水平(82.0±7.8皮摩尔/2小时),而生理盐水输注组则显著下降(至53.7±5.0皮摩尔/2小时)。在接受上述生理盐水或葡萄糖输注的另一组动物中,测定了肾乳头渗透压。生理盐水输注组的渗透压显著更高(P<0.001)。结论是,肾脏前列腺素E2合成不太可能直接参与钠稳态,且通过尿前列腺素E2排泄测定的前列腺素E2合成不受乳头渗透压控制。

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本文引用的文献

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