Alterations in lipid peroxidation of thrombin-stimulated rat platelets treated with beta-adrenoceptor blocking drugs.

Journal of lipid mediators Pub Date : 1993-10-01
R Nosál, M Petríková, V Jancinová
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引用次数: 0

Abstract

Thrombin-stimulated formation of malondialdehyde in isolated rat platelets was time- and dose-dependent and occurred in parallel with thromboxane B2 production and platelet aggregation. beta-Adrenoceptor blocking drugs inhibited thrombin-stimulated malondialdehyde formation according to their liposolubility in the rank order of potency: atenolol < practolol < oxprenolol < metipranolol approximately alprenolol approximately propranolol. In platelets pretreated with beta-blockers and stimulated with thrombin, a positive correlation was found between malondialdehyde formation and inhibition of aggregation, arachidonic acid liberation from membrane phospholipids as well as thromboxane production. Measurement of malondialdehyde was shown to be an indicator for the arachidonic acid pathway in stimulated and inhibited isolated platelets.

β -肾上腺素受体阻断药物对凝血酶刺激大鼠血小板脂质过氧化的影响。
在离体大鼠血小板中,凝血酶刺激丙二醛的形成具有时间和剂量依赖性,并与血栓素B2的产生和血小板聚集并行发生。β -肾上腺素能阻滞剂抑制凝血酶刺激丙二醛形成的效价顺序为:阿替洛尔<普萘洛尔<奥异那洛尔<美地萘洛尔近似阿替诺尔近似心得萘洛尔。在用β受体阻滞剂预处理和凝血酶刺激的血小板中,发现丙二醛的形成与聚集抑制、膜磷脂中花生四烯酸的释放以及血栓素的产生呈正相关。丙二醛的测量被证明是花生四烯酸途径在刺激和抑制分离血小板的一个指标。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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