| 丙泊酚抑制去甲肾上腺素诱导大鼠肺动脉平滑肌细胞内游离钙浓度升高作用的机理 |
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| 引用本文： | 魏敏杰,李 智,郭正东,丛 华,盛卓人. 丙泊酚抑制去甲肾上腺素诱导大鼠肺动脉平滑肌细胞内游离钙浓度升高作用的机理[J]. 中国药理学与毒理学杂志, 1999, 13(2): 127-130 |
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| 作者姓名： | 魏敏杰 李 智 郭正东 丛 华 盛卓人 |
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| 作者单位： | (中国医科大学药理学教研室; 2. 第一临床学院麻醉学教研室; 沈阳 110001) |
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| 摘 要： | 用荧光分光光度法及同位素放射免疫分析法检测丙泊酚(30-300 μmol·L-1)影响大鼠肺动脉平滑肌细胞(PASMC)内游离钙离子浓度(［Ca2+］i)与肌醇-1，4，5-三磷酸(IP3)合成作用，以探讨丙泊酚舒张肺动脉平滑肌的作用机理.结果表明，与丙泊酚共同培养72 h，对PASMC ［Ca2+］i 基础水平无明显影响，但可浓度依赖性抑制去甲肾上腺素(NE 3 μmol·L-1)引起的［Ca2+］i升高作用；当细胞外液无钙或存在钙通道阻滞剂维拉帕米(30 μmol·L-1)时，丙泊酚抑制NE升高［Ca2+］i作用被增强；丙泊酚还可浓度依赖性抑制NE促进 IP3合成作用. 结果提示丙泊酚舒张血管平滑肌作用与抑制IP3介导的细胞内钙释放密切相关.
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| 关 键 词： | 丙泊酚 肺动脉 肌,平滑,血管 肌醇-1,4,5-三磷酸 钙,游离的,细胞内 |
| 收稿时间： | 1997-11-11 |
Mechanism of propofol inhibiting norepinephrine-induced levation of intracellular free calcium in pulmonary artery smooth muscle cells of rat |
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| WEI Min-Jie, LI Zhi, GUO Zheng-Dong, CONG Hua, SHENG Zhuo-Ren. Mechanism of propofol inhibiting norepinephrine-induced levation of intracellular free calcium in pulmonary artery smooth muscle cells of rat[J]. Chinese Journal of Pharmacology and Toxicology, 1999, 13(2): 127-130 |
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| Authors: | WEI Min-Jie LI Zhi GUO Zheng-Dong CONG Hua SHENG Zhuo-Ren |
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| Affiliation: | (Department of Pharmacology, 2. Department of Anesthesiology, China Medical University, Shenyang 110001) |
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| Abstract: | To probe into the mechanism of propofol on the relaxation of the vascular smooth muscle, the effects of propofol (30-300 μmol·L-1) on intracellular free calcium concentration (［Ca2+］i) and inositol-1,4,5-triphosphate (IP3) biological synthesis induced by norepinephrine (NE 3 μmol·L-1) in pulmonary artery smooth muscle cells (PASMC) in rats were examined by using the spectrofluorometry and radioimmunoassay. The results showed that: (1) when primary cultured PASMC were pretreated with propofol for 72 h the basic levels of ［Ca2+］i did not change obviously, but the NE induced ［Ca2+］i increase was concentration dependently inhibited. (2) When in the extracellular calcium free medium or in the calcium channel blocker (verapamil 30 mmol·L-1) medium, the inhibition of propofol on NE-induced ［Ca2+］i increase was enhanced. (3) Propofol inhibited IP3 biological synthesis induced by NE in the concentration-dependent manner. These results suggest that the relaxation of propofol on pulmonary artery smooth muscle be closely related to decrease of ［Ca2+］i through mechanism of IP3 induced calcium release. |
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| Keywords: | propofol pulmonary artery muscle smooth vascular inositol- 1 4 5-triphosphate calcium free intracellular |
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