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多巴胺对犬胃内内毒素及失血性休克的影响。

Effects of dopamine on endotoxin and hemorrhagic shock in the canine stomach.

作者信息

Kuo Y J, Chou A C, Ma T W, Shanbour L L

出版信息

Circ Shock. 1977;4(2):171-80.

PMID:923016
Abstract

Studies were conducted to evaluate the effects of dopamine on gastric electrophysiopathology in endotoxin and hemorrhagic shock. Intraarterial infusion of dopamine (15.5 or 31 microgram/kg/min) in the in vivo stomach preparation produced an immediate decrease in electrical potential difference (PD), which then returned and exceeded control values. No changes in resistance (R) and blood pressure were observed. These electrophysiological responses of the gastric mucosa to dopamine are very similar to the actions of epinephrine. The in vitro studies demonstrated that active transport of Na+ was stimulated with an addition of dopamine or epinephrine (2 X 10(-4) M) to the serosal solutions of the isolated gastric mucosa. In addition, the in vivo studies demonstrated that both 40% hemorrhage and 1 mg/kg of endotoxin given as an intravenous bolus decreased PD and blood pressure and increased R although dopamine was continuously infused intraarterially for 60 minutes prior to and following hemorrhage or endotoxin. Administration of endotoxin at the onset of dopamine infusion decreased both blood pressure and PD initially. While PD showed a complete recovery at a later stage, blood pressure never returned to control levels. These results, combined with previous observations, suggest that: 1) dopamine has no beneficial action on the gastric mucosa during hemorrhagic or endotoxin shock; 2) dopamine acts on the electrophysiology in vivo and Na+ fluxes in vitro in the gastric mucosa in a manner similar to epinephrine; and 3) decrease in blood flow may be responsible for the observed decrease in transmural PD after dopamine and epinephrine in vivo.

摘要

开展了多项研究以评估多巴胺对内毒素和失血性休克时胃电生理病理的影响。在体内胃制备模型中动脉内输注多巴胺(15.5或31微克/千克/分钟)可使跨膜电位差(PD)立即降低,随后又恢复并超过对照值。未观察到电阻(R)和血压有变化。胃黏膜对多巴胺的这些电生理反应与肾上腺素的作用非常相似。体外研究表明,向离体胃黏膜的浆膜溶液中添加多巴胺或肾上腺素(2×10⁻⁴ M)可刺激Na⁺的主动转运。此外,体内研究表明,尽管在出血或内毒素给药前后均持续动脉内输注多巴胺60分钟,但静脉推注40%的失血量或1毫克/千克的内毒素均可降低PD和血压,并增加R。在多巴胺输注开始时给予内毒素最初会降低血压和PD。虽然PD在后期完全恢复,但血压从未恢复到对照水平。这些结果与先前的观察结果相结合,表明:1)在失血性或内毒素性休克期间,多巴胺对胃黏膜没有有益作用;2)多巴胺对胃黏膜体内电生理和体外Na⁺通量的作用方式与肾上腺素相似;3)血流量减少可能是体内多巴胺和肾上腺素后观察到的跨膜PD降低的原因。

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