[血栓素和白三烯在乙酰氯碱和苯肾上腺素诱导门静脉收缩反应机制中的作用]。

O O Vinogradova, P I Yanchuk, O M Pasichnichenko
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引用次数: 1

摘要

本实验研究了匹克胺和紫脲对乙酰胆碱(2.10(-5)mol/1)和苯肾上腺素(5.10(-7)mol/1)诱导的大鼠门静脉制剂强直性收缩活性的影响。内皮细胞合成花生四烯酸产物(前列腺素、白三烯)的转化在血管张力的局部调节中起重要作用。在一连串的酶转化中形成的化合物可以调节其他血管活性因子的作用。Picotamide (6,5.10(-5) mol/1) -血栓素受体和凝血素合酶阻滞剂-与对照组相比,乙酰胆碱诱导的完整内皮门静脉离体节段紧张性收缩减少29%,去甲肾上腺素诱导的收缩减少45%。所得结果表明血栓素和/或内过氧化物H2参与了该反应。5-脂氧合酶阻滞剂zileuton(4,2.10(-5) mol/1)对收缩的部分抑制作用相对于对照值为23%,表明脂氧合酶途径的产物参与了花生四烯酸转化的特定反应机制。这些数据表明门静脉血管张力调节的复杂机制,其中起重要作用的二十烷类蛋白。这些机制的进一步研究是基础知识形成的必要条件,也是阐明血管病理状况发生发展的机制及其纠正方法的发展的必要条件。
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[ROLE OF THROMBOXANE AND LEUKOTRIENES IN MECHANISMS OF CONTRACTILE REACTIONS OF PORTAL VEIN, INDUCED BY ACETYLCHLINE AND PHENYLEPHRINE].
Effects of picotamide and zileuton on tonic contractile activity of the rat portal vein preparations, induced by acetylcholine (2.10(-5) mol/1) and phenylephrine (5.10(-7) mol/1) were investigated. Conversion of arachidonic acid products (prostaglandins, leukotrienes) synthesized by endothelial cells, plays an important role in the local regulation of vascular tone. The compounds formed in a cascade of enzymatic transformations can modulate the effect of other vasoactive factors. Picotamide (6,5.10(-5) mol/1) - thromboxane receptor and thromboxane -synthase blocker - depress acetylcholine-induction tonic contraction of isolated segments of portal vein with intact endothelium by 29% and norepinephrine-induction reduction of 45% relative to the control values. The obtained results indicate a participation of thromboxane and/or endoperoxide H2 in this reaction. Partial inhibition of the contractions by 5-lipoxygenase blocker zileuton(4,2.10(-5) mol/1) at 23% relative to control values suggests, that products of lipoxigenase pathways of arachidonic acid conversion are involved in mechanisms of specified reactions. These data indicate complex mechanisms of regulation of vascular tone of the portal vein, which play an important role eicosanoids. Further study of these mechanisms is necessary for the formation of basic knowledge, as well as to elucidate the mechanisms of occurrence and development of pathological conditions of vessels and the development of methods of their correction.
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