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J Physiol. 1983 Mar;336:39-46. doi: 10.1113/jphysiol.1983.sp014564.
2
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Reduction of urinary excretion of PGE2 and 6 keto PGF1 alpha by tiaprofenic acid.噻洛芬酸降低前列腺素E2和6-酮-前列腺素F1α的尿排泄量。
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本文引用的文献

1
Composition of the renal medulla during water diuresis.水利尿期间肾髓质的组成。
J Clin Invest. 1962 May;41(5):1145-51. doi: 10.1172/JCI104567.
2
COMPOSITION OF THE RENAL CORTEX AND MEDULLA OF RATS DURING WATER DIURESIS AND ANTIDIURESIS.大鼠水利尿和抗利尿期间肾皮质和髓质的组成
Q J Exp Physiol Cogn Med Sci. 1965 Apr;50:146-57. doi: 10.1113/expphysiol.1965.sp001777.
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Stimulation of the sodium-potassium pump by trypsin in low potassium type erythrocytes of goats.胰蛋白酶对山羊低钾型红细胞钠钾泵的刺激作用。
J Physiol. 1980 Apr;301:25-37. doi: 10.1113/jphysiol.1980.sp013185.
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Is urinary flow rate a major regulator of prostaglandin E excretion in man?尿流率是人类前列腺素E排泄的主要调节因素吗?
Prostaglandins Med. 1980 May;4(5):303-9. doi: 10.1016/0161-4630(80)90003-8.
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Sodium intake as a determinant of urinary prostaglandin E2 excretion.
Prostaglandins Med. 1980 Jan;4(1):53-63. doi: 10.1016/0161-4630(80)90063-4.
6
Renal function in conscious rats after indomethacin. Evidence for a tubular action of endogenous prostaglandins.消炎痛作用后清醒大鼠的肾功能。内源性前列腺素肾小管作用的证据。
J Physiol. 1980 Jan;298:371-81. doi: 10.1113/jphysiol.1980.sp013087.
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Dissociation between renal medullary PGE2-synthesis and urine PGE2-excretion. Antagonism by bumetanide of chlorazanil induced urine PGE2-excretion in rats.
Prostaglandins. 1981 Apr;21(4):591-7. doi: 10.1016/0090-6980(81)90007-1.
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Renal prostaglandins and sodium excretion.肾前列腺素与钠排泄
Q J Exp Physiol. 1982 Jul;67(3):377-85. doi: 10.1113/expphysiol.1982.sp002652.
9
Role of prostaglandins in mediating excretion by the kidney of an intravenous infusion of sodium chloride in normal human subjects.
Clin Sci (Lond). 1982 Jan;62(1):27-33. doi: 10.1042/cs0620027.
10
Effect of chronic and acute changes in sodium balance on the urinary excretion of prostaglandins E2 and F2 alpha in normal man.钠平衡的慢性和急性变化对正常男性尿中前列腺素E2和F2α排泄的影响。
Clin Sci (Lond). 1981 Apr;60(4):405-10. doi: 10.1042/cs0600405.

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.

DOI:10.1113/jphysiol.1983.sp014564
PMID:6576130
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1198953/
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。