Halothane, but not α-chloralose, blocks potassium-evoked cortical spreading depression in cats

Halothane, but not α-chloralose, blocks potassium-evoked cortical spreading depression in cats
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氟烷(而非 α-氯醛糖)可以阻止钾引起的猫皮质扩散性抑制

DOI:
10.1016/0006-8993(95)00898-z
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发表时间:
1995
期刊:
影响因子:
2.9
通讯作者:
W. Heiss
W. Heiss
中科院分区:
医学3区
文献类型:
--
作者:
R. Saito;R. Graf;K. Hübel;J. Taguchi;G. Rosner;T. Fujita;W. Heiss

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在人工通气(30% 氧气/70% 一氧化二氮)猫中研究了两种麻醉剂(氟烷和 α-氯醛糖)对皮内注射钾后诱导扩散性抑制和细胞外谷氨酸升高的影响。使用直接 KCl 注射(7 μl,通过微量移液器 150 mM)或微透析通过分别向灌注溶液(Ringer's)补充 100、300 或 500 mM KCl 10 分钟来实现高钾浓度。记录注射部位附近(1-2 毫米:电极 DC1)和远处(6-7 毫米:电极 DC2)的皮质直流电位变化。在氟烷(呼吸气体混合物中 0.75%)或 α-氯醛糖(60 mg/kg 静脉注射)麻醉下,在注射部位(电极 DC1)附近测量反映 KCl 注射后钾水平升高的 DC 电位的长时间负移。相比之下,几乎只在 α-氯醛糖下观察到扩散凹陷(瞬时短 DC 偏转)。用电极 DC1 记录的扩散凹陷叠加在长时间的负 DC 偏移上,并且它们频繁传播到更远的位置 (DC2)。施用 KCl 后,测量了细胞外谷氨酸的剂量依赖性升高。这些升高并未因麻醉类型而显着改变。我们的结果表明,在猫中,扩散性抑郁诱导受到麻醉的影响,即与α-氯醛糖相比,氟烷抑制扩散性抑郁诱导。此外,谷氨酸或高钾以外的因素似乎也有助于抑郁诱导的传播。
The effects of two anesthetics, halothane and α-chloralose, on induction of spreading depression and on extracellular glutamate elevation after intracortical potassium administration were investigated in artificially ventilated (30% oxygen/70% nitrous oxide) cats. High potassium concentrations were achieved using either direct KCl injections (7 μl, 150 mM via a micropipette) or microdialysis by supplementing 100, 300 or 500 mM KCl, respectively, for 10 min to the perfusion solution (Ringer's). Changes of the cortical DC potential were recorded adjacent (1–2 mm: electrode DC1) and distant (6–7 mm: electrode DC2) to the injection site. Either under halothane (0.75% in the respiratory gas mixture) or under α-chloralose (60 mg/kg i.v.) anesthesia, prolonged negative shifts of the DC potential reflecting the elevated potassium levels after KCl injection were measured near the injection site (electrode DC1). In contrast, spreading depressions (transient short DC deflections) were almost exclusively observed under α-chloralose. Spreading depressions recorded with electrode DC1 were superimposed on the prolonged negative DC shifts and they propagated frequently to the more distant site (DC2). Upon KCl administration, dose dependent elevations of extracellular glutamate were measured. These elevations were not significantly altered by the type of anesthesia. Our results suggest that in cats, spreading depression induction is affected by anesthesia, i.e., spreading depression induction is inhibited by halothane as compared to α-chloralose. Furthermore, factors other than glutamate or high potassium seem to contribute to spreading depression induction.