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[丙泊酚和硫喷妥钠对培养的大鼠主动脉平滑肌细胞中尼可地尔诱导的ATP敏感性钾通道活性的影响]

[Effects of propofol and thiamylal on nicorandil induced ATP-sensitive potassium channel activities in cultured rat aortic smooth muscle cells].

作者信息

Eguchi Satoru, Kawano Takashi, Oshita Shuzo, Nakajo Nobuyoshi

机构信息

Department of Dental Anesthesiology, Tokushima University School of Dentistry.

出版信息

Masui. 2005 Apr;54(4):364-9.

Abstract

BACKGROUND

Nicorandil, a hybrid ATP-sensitive potassium (K(ATP)) channel opener and nitrate compound, is used clinically for the treatment of angina pectoris. In the present study, we investigated the effects of propofol and thiamylal on sarcolemmal K(ATP) channels activities induced by nicorandil in cultured rat aortic smooth muscle cells.

METHODS

We used inside-out patch clamp configurations to investigate the effects of propofol and thiamylal on nicorandil induced K(ATP) channel activities.

RESULTS

K(ATP) channel was not spontaneously activated by patch excision in the absence of intracellular ATP. Application of nicorandil (100 microM) induced a marked activation of KATP channel currents, which was completely blocked by 3 microM glibenclamide, the sulfonylurea that blocks K(ATP) channels. Nicorandil induced KATP channel currents were not significantly inhibited by application of 10 and 100 microM propofol to intracellular surface. However, application of 100 and 300 microM thiamylal to intracellular surface significantly inhibited the nicorandil induced K(ATP) channel currents, with relative channel activities decreasing to 0.65 +/- 0.08 and 0.46 +/- 0.10 of control, respectively.

CONCLUSIONS

Propofol had no effect on nicorandil induced sarcolemmal KATP channel activities in rat aortic smooth muscle cells, whereas thiamylal significantly inhibited these channel activities at clinically relevant concentrations.

摘要

背景

尼可地尔是一种兼具ATP敏感性钾(K(ATP))通道开放剂和硝酸盐化合物特性的药物,临床上用于治疗心绞痛。在本研究中,我们调查了丙泊酚和硫喷妥钠对尼可地尔诱导的培养大鼠主动脉平滑肌细胞肌膜K(ATP)通道活性的影响。

方法

我们采用内面向外式膜片钳配置来研究丙泊酚和硫喷妥钠对尼可地尔诱导的K(ATP)通道活性的影响。

结果

在没有细胞内ATP的情况下,膜片钳切除不会自发激活K(ATP)通道。应用尼可地尔(100微摩尔)可显著激活KATP通道电流,该电流被3微摩尔格列本脲(一种阻断K(ATP)通道的磺酰脲类药物)完全阻断。向细胞内表面施加10和100微摩尔丙泊酚对尼可地尔诱导的KATP通道电流没有显著抑制作用。然而,向细胞内表面施加100和300微摩尔硫喷妥钠可显著抑制尼可地尔诱导的K(ATP)通道电流,相对通道活性分别降至对照的0.65±0.08和0.46±0.10。

结论

丙泊酚对尼可地尔诱导的大鼠主动脉平滑肌细胞肌膜KATP通道活性没有影响,而硫喷妥钠在临床相关浓度下可显著抑制这些通道活性。

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