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多巴胺受体阻断并不影响狗输注氯化钠时伴随出现的利钠作用。

Dopamine receptor blockade does not affect the natriuresis accompanying sodium chloride infusion in dogs.

作者信息

Bradley T, Gewertz B L, Scott W J, Goldberg L I

出版信息

J Lab Clin Med. 1986 Jun;107(6):525-8.

PMID:2940307
Abstract

Intravenous (IV) saline infusions cause parallel increments in urinary excretion of dopamine (DA) and sodium. Exogenous administration of DA exerts a natriuretic effect by action on DA receptors. The possibility that DA mediates the natriuretic response to saline infusion was studied by infusing 0.9% saline solution IV (60 ml/kg) in conscious dogs with and without selective blockade of DA1 and DA2 receptors. With no antagonist, the total increase in sodium excretion during the 120-minute saline infusion and the 60 minutes after the saline infusion was 99.5 +/- 7.6 mmol. The increase in total sodium excretion was not affected by IV infusion of the selective DA1 antagonist SCH 23390 in doses of 0.5 micrograms/kg/min and 5 micrograms/kg/min. The total increment in sodium excretion produced by saline was also unaltered by large doses (1 micrograms/kg/min and 10 micrograms/kg/min) of the selective DA2 antagonist domperidone. Our results do not support a role of DA as a mediator of saline-induced natriuresis in the dog.

摘要

静脉输注生理盐水会使多巴胺(DA)和钠的尿排泄量平行增加。外源性给予多巴胺通过作用于多巴胺受体发挥利钠作用。通过对清醒犬静脉输注0.9%生理盐水溶液(60 ml/kg),同时选择性阻断或不阻断DA1和DA2受体,研究了多巴胺介导生理盐水输注所致利钠反应的可能性。在无拮抗剂的情况下,在120分钟生理盐水输注期间及输注后60分钟内,钠排泄总量增加99.5±7.6 mmol。静脉输注剂量为0.5微克/千克/分钟和5微克/千克/分钟的选择性DA1拮抗剂SCH 23390,钠排泄总量的增加不受影响。大剂量(1微克/千克/分钟和10微克/千克/分钟)的选择性DA2拮抗剂多潘立酮也未改变生理盐水所致钠排泄总量的增加。我们的结果不支持多巴胺在犬中作为生理盐水诱导利钠作用介质的作用。

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