氟烷抑制二苯撑碘鎓的升压作用。

Halothane inhibits the pressor effect of diphenyleneiodonium.

作者信息

Wang Y X, Pang C C

机构信息

Department of Pharmacology & Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.

出版信息

Br J Pharmacol. 1993 Aug;109(4):1186-91. doi: 10.1111/j.1476-5381.1993.tb13747.x.

DOI:10.1111/j.1476-5381.1993.tb13747.x

PMID:8401928

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2175759/

Abstract

We have recently found that diphenyleneiodonium (DPI), a novel inhibitor of nitric oxide (NO) synthase, causes pressor and tachycardic responses in pentobarbitone- but not halothane-anaesthetized rats. The present study investigated the mechanism by which halothane suppresses the pressor response of DPI. The effects of halothane on the pressor response of DPI were also compared with those of other anaesthetic agents. 2. In conscious rats, i.v. bolus injections of DPI (0.025- 1.6 mg kg-1) caused dose-dependent increases in mean arterial pressure (MAP), with ED90 of 0.07 +/- 0.01 mg kg-1 and maximal rise of MAP (Emax) of 59 +/- 2 mmHg. While ketamine potentiated Emax without altering the ED50 and pentobarbitone increased the ED50 without changing Emax of the pressor response to DPI, chloralose, urethane and ethanol displaced the curve to the right and potentiated Emax. In contrast, halothane (0.5-1.25%) dose-dependently and non-competitively reduced the pressor responses to DPI. 3. Intravenous bolus injection of a single dose of DPI (1.6 mg kg-1) caused immediate and large increases in plasma noradrenaline and adrenaline, as well as MAP in conscious rats. Halothane (1.25%) almost completely inhibited these increases. 4. The results suggest that DPI causes a pressor response in conscious rats by activating the sympathetic nervous system and halothane abolishes this pressor response by inhibiting activities of the sympathetic nervous system. The results also show that influences of anaesthetics must be taken into consideration when evaluating pressor response of vasoactive agents.

摘要

我们最近发现，二亚苯基碘鎓（DPI）是一种新型一氧化氮（NO）合酶抑制剂，在戊巴比妥麻醉而非氟烷麻醉的大鼠中会引起升压和心动过速反应。本研究调查了氟烷抑制DPI升压反应的机制。还将氟烷对DPI升压反应的影响与其他麻醉剂的影响进行了比较。2. 在清醒大鼠中，静脉推注DPI（0.025 - 1.6 mg kg⁻¹）可使平均动脉压（MAP）呈剂量依赖性升高，ED90为0.07 ± 0.01 mg kg⁻¹，MAP最大升高值（Emax）为59 ± 2 mmHg。氯胺酮增强了Emax但未改变ED50，戊巴比妥增加了ED50但未改变对DPI升压反应的Emax，氯醛糖、乌拉坦和乙醇使曲线右移并增强了Emax。相比之下，氟烷（0.5 - 1.25%）剂量依赖性且非竞争性地降低了对DPI的升压反应。3. 静脉推注单剂量DPI（1.6 mg kg⁻¹）可使清醒大鼠的血浆去甲肾上腺素和肾上腺素立即大幅增加，同时MAP也升高。氟烷（1.25%）几乎完全抑制了这些增加。4. 结果表明，DPI通过激活交感神经系统在清醒大鼠中引起升压反应，而氟烷通过抑制交感神经系统的活动消除了这种升压反应。结果还表明，在评估血管活性药物的升压反应时，必须考虑麻醉剂的影响。