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黑种草(Nigella sativa)挥发油对大鼠的心血管作用:作用机制的阐释

The cardiovascular actions of the volatile oil of the black seed (Nigella sativa) in rats: elucidation of the mechanism of action.

作者信息

el Tahir K E, Ashour M M, al-Harbi M M

机构信息

Department of Pharmacology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.

出版信息

Gen Pharmacol. 1993 Sep;24(5):1123-31. doi: 10.1016/0306-3623(93)90359-6.

Abstract
  1. The effects of the volatile oil (V.O.) of the black seed (Nigella sativa) on the arterial blood pressure and heart of urethane-anaesthetized rats were investigated and the effects were compared with those of its constituent thymoquinone (T.Q.). 2. Intravenous administration of V.O. in the dose range (4-32 microliters kg.-1) or T.Q. (0.2-1.6 mg kg-1) to rats decreased the arterial blood pressure and the heart rate in a dose-dependent manner. 3. The effects of V.O. were significantly antagonized by treatment of the animals with cyproheptadine, hexamethonium atropine and by spinal pithing. 4. Treatment of the animals with reserpine (5 mg kg- 1 day-1 for 2 days) significantly antagonized the cardiovascular depressant effects induced by 4 and 8 microliters of V.O. kg-1 but not those induced by the larger doses. 5. T.Q.-induced cardiovascular depressant effects were significantly antagonized by atropine and cyproheptadine but not by reserpine. 6. The results suggested that V.O.-induced cardiovascular depressant effects were mediated mainly centrally via indirect and direct mechanisms that involved both 5-hydroxytryptaminergic and muscarinic mechanisms. The direct mechanisms may be due to the presence of T.Q. in the V.O. The V.O. seemed to possess the potential of being a potent centrally acting antihypertensive agent.
摘要
  1. 研究了黑种草(Nigella sativa)挥发油(V.O.)对乌拉坦麻醉大鼠动脉血压和心脏的影响,并将其与成分百里醌(T.Q.)的影响进行了比较。2. 给大鼠静脉注射剂量范围为4 - 32微升/千克的V.O.或0.2 - 1.6毫克/千克的T.Q.,会使动脉血压和心率呈剂量依赖性降低。3. 用赛庚啶、六甲铵、阿托品处理动物以及脊髓切断术可显著拮抗V.O.的作用。4. 用利血平(5毫克/千克·天,连续2天)处理动物可显著拮抗4微升/千克和8微升/千克V.O.诱导的心血管抑制作用,但对较大剂量诱导的作用无此效果。5. 阿托品和赛庚啶可显著拮抗T.Q.诱导的心血管抑制作用,但利血平无此作用。6. 结果表明,V.O.诱导的心血管抑制作用主要通过间接和直接机制在中枢介导,涉及5 - 羟色胺能和毒蕈碱能机制。直接机制可能归因于V.O.中存在T.Q.。V.O.似乎具有成为一种强效中枢性抗高血压药物的潜力。

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