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正常志愿者静脉注射氯化钠负荷后钠排泄的体液决定因素。

Humoral determinants of Na+ excretion after intravenous NaCl loading in normal volunteers.

作者信息

Stokes G S, Johnston H J, Monaghan J C

机构信息

Department of Clinical Pharmacology, Royal North Shore Hospital, St Leonards, New South Wales, Australia.

出版信息

Clin Exp Pharmacol Physiol. 1993 May;20(5):310-2. doi: 10.1111/j.1440-1681.1993.tb01691.x.

Abstract
  1. Twelve healthy volunteers maintained on a 100 mmol/day Na+ diet, were given an intravenous infusion of 2L saline (0.9%) between 10.00 h on 2 study days at least 1 week apart. Urine collections (90 min) were made from 08.30 to 16.00 h. Either carbidopa 100 mg or indomethacin 50 mg was given orally at 07.45 h on one study day and placebo was given on the other (in random order). 2. On the placebo day, saline infusion caused significant decreases in plasma albumin concentration, plasma renin activity (PRA), plasma aldosterone concentration and urinary aldosterone excretion, with 2 to 3-fold increases in plasma atrial natriuretic peptide (ANP) concentration and urinary dopamine: noradrenaline ratio (DA:NA), whereas mean urinary kallikrein and prostaglandin E2 (PGE2) excretion rates were unchanged. Carbidopa decreased urinary DA:NA and indomethacin decreased urinary PGE2 excretion, compared with the placebo day. Excretion of sodium (Na+) decreased below baseline in two out of six carbidopa-treated subjects and in three out of six indomethacin-treated subjects, but showed little or no change in the remainder. 3. These preliminary observations suggest that some subjects in the early phase of natriuresis after an intravenous Na+ load can be identified as having prostaglandin-dependent or dopamine-dependent mechanisms for Na+ excretion.
摘要
  1. 12名维持100 mmol/天钠饮食的健康志愿者,在至少相隔1周的2个研究日的10:00时接受2升生理盐水(0.9%)静脉输注。在08:30至16:00时收集尿液(90分钟)。在一个研究日的07:45时口服卡比多巴100毫克或吲哚美辛50毫克,另一研究日给予安慰剂(随机顺序)。2. 在给予安慰剂的日子里,输注生理盐水导致血浆白蛋白浓度、血浆肾素活性(PRA)、血浆醛固酮浓度和尿醛固酮排泄显著降低,血浆心房利钠肽(ANP)浓度和尿多巴胺:去甲肾上腺素比值(DA:NA)增加2至3倍,而尿激肽释放酶和前列腺素E2(PGE2)平均排泄率未改变。与给予安慰剂的日子相比,卡比多巴降低了尿DA:NA,吲哚美辛降低了尿PGE2排泄。在接受卡比多巴治疗的6名受试者中有2名以及接受吲哚美辛治疗的6名受试者中有3名,钠(Na+)排泄低于基线水平,但其余受试者变化很小或无变化。3. 这些初步观察结果表明,静脉注射钠负荷后处于利钠早期阶段的一些受试者可被确定为具有依赖前列腺素或多巴胺的钠排泄机制。

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